Oscillatory Thoughts

Gladwellified Writing

2012-02-10T09:35:00.000-08:00

What X can teach us about Y

So I noticed a trend today while reading through some articles wherein titles follow the above format with surprising frequency. A little Google digging shows that this is all over the place, and that I'm not the only one that's noticed!

What's amusing is that my first thought when I noticed this was "GLADWELL!!!!" ::shakes fist::

The Salon author also mentions Gladwell and Freakonomics as likely causes for this cliche. What is it about these "connections" that get people so excited and draws them in?

As proof, here's a Gladwell piece following the WXCTUAY format:

Okay, okay, here's real proof:
Troublemakers: What pit bulls can teach us about profiling

I'm just going to go ahead and add WXCTUAY to my list of things I wish journalists would stop doing. No, scientists don't really "pinpoint" stuff, no, you don't need to add neuroscience nonsense to your story to "sex it up", and no, X doesn't teach us anything about Y, because X is an inanimate object or ephemeral concept.

WXCTUAY abounds, with 126 books on Amazon using it.

Here are some quick ones from around the web:
• What The Wizard of Oz Can Teach Us about Bullying
• What Frank Herbert's Dune Can Teach Us About the Power of Positive Thinking
• What Bartleby Can Teach Us About Occupy Wall Street
• What Sweden can teach us about nuclear waste
• 2 Things Charles Dickens Can Teach Us about Successful Presentations
• What Mel Brooks Can Teach Us about "Group Flow"
• Managing the Clock: What Sports Can Teach Us About Life
• What the Scots can teach us about England's radical soul
• What Pictures Can Teach Us About Walkability

Amusingly, though Salon called out this trend, they're quite enamored with WXCTUAY as well! Two quick examples:
• What "Star Wars" can teach my son about life
• What students can teach us about iPhones

Anyone out there seen any especially silly ones?

Basic science is about creating opportunities

2012-02-09T14:08:00.000-08:00

Did you know that US House Majority Leader Eric Cantor runs a website called "YouCut" that encourages citizens to submit "questionable" NSF grants that should lose their funding?

Step One: Look for Questionable Grants
Click here to open the National Science Foundation website. In the "Search Award For" field, try some keywords, such as: success, culture, media, games, social norm, lawyers, museum, leisure, stimulus, etc. to bring up grants. If you find a grant that you believe is a waste of your taxdollars, be sure to record the award number.

First, check out those suggested key words. "Social norms", "culture", "success"...? Do these terms hold some secret, coded meaning among the anti-science crowd that I just don't get?

What's wrong with this? What's wrong with cutting funding to projects such as "shrimp walking on a tiny treadmill" and "a robot folding laundry"? Saving taxpayer money is a good thing, and I genuinely respect efforts to do so.

But these "frivolous" projects don't exist in a vacuum.

You can't legislate innovation and you can't democratize a breakthrough. You can, however, create a system that maximizes the probability that a breakthrough can occur.

We scientists stand on the shoulders of giants. The more research you fund, the more giants we get, and the pyramid of giants standing on giants grows ever larger. (Okay, that metaphor broke down at the end there...)

Scicurious did a good takedown of one of Tom Coburn's "Wastebook" listed projects over on the Scientific American blogs, but I want to compile a whole list of projects.

Here is my list of "really stupid, frivolous academic pursuits" that have lead to major scientific breakthroughs. If you know of any more, I'd love to hear about them. I'd like to compile a list to use as ammunition in the future, because Cantor certainly isn't the first--nor will he be the last--federal politician to play this game.

• Studying monkey social behaviors and eating habits lead to insights into HIV (Radiolab: Patient Zero)
• Research into how algae move toward light paved the way for optogenetics: using light to control brain cells (Nature 2010 Method of the Year).
• Black hole research gave us WiFi (ICRAR award)
• Optometry informs architecture and saved lives on 9/11 (APA Monitor)
• Certain groups HATE SETI, but SETI's development of cloud-computing service SETI@HOME paved the way for citizen science and recent breakthroughs in protein folding (Popular Science)
• Astronomers provide insights into medical imaging (TEDxBoston: Michell Borkin)
• Basic physics experiments and the Fibonacci sequence help us understand plant growth and neuron development:

Here's a link to a Google Doc for these projects! Please feel free to add more, and remember to reference it in the future.

What I love about these is that so many started from canonical "wasteful spending" types of "pointless" research: astronomy and black holes, studying algae, SETI, etc.

The ideas spawned from these basic projects could never have been anticipated. We don't do the research that will lead to the best immediate applications, we do the research that is interesting because it is interesting. The possibility for a breakthrough can't exist if we stop supporting basic research because it "feels" silly.

Science shouldn't be seen as a zero-sum game.

(h/t to Ecogirl & Cosmoboy's blog for the astronomy stuff!)

PubMeddler

2012-02-03T13:22:00.000-08:00

I made a thing this morning. It's a Markov text generator of PubMed papers. Messing with PubMed for to make best science.

Here's the tumblr for it, and its twitter.

For the first one I used the seed term "elegans:

Functional genomics, to gain insights into the maternal pool

The recombinant protein could recognize excretory-secretary antigens from Angiostrongylus cantonensis third-stage larvae (L3). Also, the antiserum can recognize larval soluble antigens of L4 coming from mice (nonpermissive host) infected with virulent Legionella strains were exposed to chlorpyrifos. Hence, the loss of ifg-1 p170 mRNA was caspase (ced-3) and apoptosome (ced-4/Apaf-1) dependent. These findings demonstrate that overexpression of mir-84. Mutations in the egg laying-deficient (Egl-d) and hyperactive egg laying (Egl-c). The defect in the nematode C. elegans offers the prospect of being adopted in the CNS of HFD animals possibly contributing to the head and tail.

What are some of the most surprising things that can damage someone's brain?

2012-01-30T10:12:00.000-08:00

This is another post inspired by an answer I left on Quora. This is all stuff I learned about from teaching neuroanatomy for three semesters.

WARNING! NOT FOR THE SQUEAMISH!

Neurocysticercosis

This is an infection cause by the tapeworm Taenia solium. After eating infected, undercooked pork, the tapeworm's eggs can migrate into the brain and/or other tissues where the larvae develop and mature, leaving behind cysts.

Moral of the disease: cook your pork.

Central pontine myelinolysis

This is a disorder almost always caused by an incorrect treatment of a basic disorder: hyponatremia. Hyponatremia literally means "below natrium", or too little sodium. This can be caused by many situations such as prolonged diarrhea or vomiting with too much water intake without enough electrolytes (e.g., sodium).

If a patient presents hyponatremic the obvious treatment is to give the patient sodium solution. However if the doctor tries to correct the sodium levels back to normal too quickly it may result in central pontine myelinolysis.

What this means is that the pons (part of the brainstem) loses myelin (the insulating wrapping around the axons of the neurons). This can lead to a mind-blowing disorder known as "locked-in syndrome" wherein the person is conscious, awake, and aware, but cannot interact with the outside world.

If you haven't read it or seen the movie, I highly recommend The Diving Bell and the Butterfly, a book written by former journalist and Elle editor-in-chief Jean-Dominique Bauby, who had locked-in syndrome.

He wrote the book by using his eyes to select a letter, one letter at a time.

Wernicke–Korsakoff syndrome

This disorder is usually induced by prolonged alcohol abuse, but is actually caused by a thiamine (vitamin B1) deficiency associated with poor nutrition in severe, long-term alcoholics.

For some reason, neurons in the mammillary bodies are especially susceptible to thiamine deficiency, causing them to preferentially die off. The mammillary bodies are heavily interconnected with the hippocampuses, and when damaged can cause severe anterograde amnesia as was seen in patient H.M. (and portrayed very oddly in the movie Memento).

As with central pontine myelinolysis, this disorder can also be caused by a physician. For example, if a patient is in a long-term coma and are not being given IV thiamine, they patient may awaken with Wernicke–Korsakoff. A "banana bag" (an IV solution containing a multi-vitamin solution including thiamine, so-called because of its yellow color) should be used for such patients. I've been told that experienced doctors will look in on comatose patients from time to time just to make sure their IV solution is yellow.

MPTP Toxicity

This is an odd case that lead to a breakthrough in neuroscientific and neurology research for disease treatment.

In 1982, seven young people in Santa Clara County were diagnosed with Parkinson's Disease. Parkinson's is very rare in people under the age of 40.

Turned out, all of these people were heroin users, and their particular batch of "synthetic" heroin (MPPP), it was later discovered, contained an impurity: MPTP.

MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) selectively destroys dopaminergic neurons in the substantia nigra, the same neurons that degenerate in Parkinson's Disease.

MPTP is actually now synthesized and used as an animal-model of Parkinson's Disease to aid in understanding and treating the disease.

Radio Interview: Wired for Thought

2012-01-18T09:03:00.000-08:00

Last week I did an interview with Molly Bentley from the SETI radio show Big Picture Science and the episode is NOW ONLINE.

This is super cool to me because the other guests include Michael freakin' Gazzaniga, Art "my hero at UCLA" Toga, and Jan "I don't know him so don't have a cutesy nickname" Rabaey.

Whaaaaat.

The episode in which I appeared was titled "Wired for Thought".

Here's their blurb:

A cup of coffee can leave you wired for the day. But a chip in your brain could wire you to a machine forever. Imagine manipulating a mouse without moving a muscle, and doing a Google search with your mind. Welcome to the future of the brain-machine interface.

Don your EEG thinking-cap, and discover a high-tech thought game that may be the harbinger of machine relationships to come.

Plus, the ultimate mapping project: the Human Connectome Project aims to identify all the neural pathways in the human brain. It may help us understand what makes us human, but could it also point the way to making us smarter?

And, what all this brain research reveals about the mind and free will – who, or what, is really in charge?

Anyway, give it a listen. I'm on for about 10 minutes around 19 minutes in.

And I don't think I suck.

I tried to do the right balance between interesting, honest, and accurate... but I'd really like to hear how others think I did. I'm not a fan of feel-good pop neuroscience, but at the same time I really want to convey to the public how exciting I think the field is because of how hard it is.

Because (at this point) I don't think this will be my last media appearance, I'd really like feedback.

In case you're wondering (because I am), I assume I'm on this episode for my hemicraniectomy/BCI research, but who knows?

A Time article that literally makes my brain lobes explode

2012-01-11T10:30:00.000-08:00

Time has just published the most frustratingly annoying piece of neurobabble I've come across (thanks for pointing me to it Avgusta!).

What I'm about to say is hard for me, because I love Time; they've twice named me their person of the year, and I hate to bite the hand that feeds me.

But forget it... that New York Times piece that I was annoyed about from this weekend has got nothing on this one.

It's a "very timely piece" about John Edwards. Is Time confused? They do know the American media is only supposed to talk about Republican presidential candidates right now, right?

Anyway, the very first sentence of the article sets the scientific tone.

John Edwards is the putrefied meat of the American political system — literally, as far as your brain is concerned.

Really? According to my brain Edwards is literally putrefied meat?

Allow me introduce you to grammar, as explained by the Oatmeal:

The article then goes on to say:

Think about Edwards for a moment — the perfect hair, the honey voice, the oleaginous smile. Your lip curled ever so slightly, didn't it? A teensy bit of bile may have risen in your throat. The lip curl is a threat display, the bile is an attempt to purge a toxin. Both were triggered at least partly by your prefrontal cortex and your temporal lobes — and both would have also occurred if you'd smelled a piece of food gone bad.

Okay, so the author asks me to think about Edwards and then tells me what my reaction should have been (my lip curled and bile rose in my throat? Has that ever happened to anyone ever?) and then tells me that my imaginary responses reflect some nonsense from my prefrontal cortex and temporal lobes (i.e., half my brain).

Okey dokey.

There's some blah blah requisite crap about fMRI, some terrible quotations from psychology faculty who are overstepping their research by talking about political outcomes, and then some amusing bits:

Edwards, a bad guy who cheated a sickly and suffering woman, practically makes our brain lobes explode.

Paradoxically, the more his critics — to say nothing of his prosecutors — are seen to be piling on, the more our temporal lobes and prefrontal cortices may switch the valence once more, turning even a deeply loathed perpetrator into an unlikely victim.

Journalists, please take heed: don't do this kind of stuff. These bits about neuroscience add nothing to the story at all, and in fact the only reason they're in here is most likely to add an air of authority (as McCabe and Castel have demonstrated... see what I did there?).

The story would have been relatively fine if it had focused on the solid psychology research into how peoples' perceptions of attractiveness affects their decision making. Instead the author threw in some loose neurononsense that cheapened the piece.

McCabe DP, & Castel AD (2008). Seeing is believing: the effect of brain images on judgments of scientific reasoning. Cognition, 107 (1), 343-52 PMID: 17803985

The New York Times on the "Cognitive Neuroscience REVOLUTION"

2012-01-08T08:07:00.000-08:00

The New York Times is at it once again in their Opinion Pages, this time with a book advertisement titled "Seeing the Building for the Trees".

It starts out with an all-caps pronouncement, which cognitive neuroscience has taught me means what is being said is VERY SERIOUS BUSINESS:

A REVOLUTION in cognitive neuroscience is changing the kinds of experiments that scientists conduct, the kinds of questions economists ask and, increasingly, the ways that architects, landscape architects and urban designers shape our built environment.

(EDIT: It's been pointed out to me that the all-caps beginning is a NYT style convention, however as a cognitive neuroscientist it's clear to me that the author is subverting the standard convention of all-caps to her own purpose because prefrontal cortex, evolutionary psychology, dopamine.)

The article then goes on to say that... embodied cognition tells us that our heads are in the clouds, therefore architecture is like trees and that, something... something... Avatar?

Honestly I don't get the neuroscience connection at all.

This metaphorical, embodied quality shapes how we relate to abstract concepts, emotions and human activity. Across cultures, "important" is big and "unimportant" is small, just as your caretakers were once much larger than you. Sometimes your head is "in the clouds." You approach a task "step by step."

Some architects are catching on to human cognition's embodied nature. A few are especially intrigued by metaphors that express bodily experience in the world.

Take the visual metaphor of a tree as shelter. Most people live around, use and look at trees. Children climb them. People gather under them. Nearly everyone at some point uses one to escape the sun.

That's a direct quote, from one paragraph to the next, in the appropriate order in which they appear in the article. I have not removed any words, rearranged any text, or done anything but hit ctrl-c and then ctrl-v.

The logic connecting one paragraph to the next--and one idea to the next--escapes me.

Even the author abandons the whole "cognitive neuroscience" device somewhere half-way through the article, and instead says something more likely grounded in reality:

Architects may also like tree metaphors because a tree's overall structure is regular, while its fine-grained composition, its tangles of branches, are irregular, an arrangement conducive to the kind of design experimentation offered by new digital technologies.

No need for any cognitive neuroscience here! Hell, by the end the author admits that the cognitive neuroscience angle may not even exist:

How many designers are clued in to the ongoing cognitive revolution and its potential for the built environment is unclear.

Blah. Whatever.

I'm too confused to even be annoyed enough to write a rebuttal. At least the New York Times iPhone piece that Russ Poldrack so deftly countered (and that I signed) was a coherent misapplication of neuroscience.

This latest Avatar, neuroscience, architecture piece is at least as silly as their "neuroscientists go canoeing" article. Or whatever that one was about.

Maybe they've got some pop-neuro quota to fulfill?

5 Reasons to Love Academia

2012-01-04T13:17:00.000-08:00

1. Freedom to set your own schedule
Academia's not a 9 to 5, cubicle slave job! We didn't go to school for 20+ years to work a measly 8 hours per day for 40 hours a week.

You see, there's a certain... "culture"... of academia that equates "good, smart work" with "endless hours in the lab".

This kind of mentality leads to famous suggestions such as the following from my PhD institute (also referenced in Nature):

1. Every one works at least 50 hr a week in the lab (e.g., 8+ hr a day, six days a week). This is by far lower than what I am doing every day and throughout most of my career. You may be smarter or do not want to be as successful, but I am not asking you to match my time in the lab

2. By working, I mean real bench work... I suggest that everyone puts in at least 6 hr concentrated bench work and 2+ hr reading and other research-related activity each day. Reading papers and books should be done mostly after work. More time can be spent on reading, literature search and writing during working hours when you are ready for writing a paper....

I expect everyone to have made sufficient progress in the research so that a good paper is in sight (at least to the level of J. Neuroscience). If you cannot meet this goal at that time, I will have to ask you to prepare to leave my lab by the end of August.

Or this gem from Caltech:

I have noticed that you have failed to come in to lab on several weekends, and more recently have failed to show up in the evenings. Moreover, in addition to such time off, you recently requested some vacation. I have no problem with vacation time that is well earned, but I do have a problem with continuous vacation and time off that interferes with the project. I find this very annoying and disruptive to your science.

I expect you to correct your work-ethic immediately.

I receive at least one post-doctoral application each day from the US and around the world. If you are unable to meet the expected work-schedule, I am sure that I can find someone else as an appropriate replacement for this important project.

You may be a unique and beautiful snowflake when you're being recruited, but once you're in, you stay in, science slave!

2. Swimming in your pools of money
Seriously though, the time spent in lab is worth it. If for no other reason than the strong pay. Why go into industry when you can make $28-30,000 per year during your 4-7 year PhD, especially when that will be followed up by 1-5 years as a post-doc making upwards of almost $39,000 annually?!

Look at those Ivory Towers!

So sketch up some quick grant on climate change and make it rain!

"What a strange business this is: We stay in school forever. We have to battle the system with only a one in eight or one in ten chance of getting funded. We give up making a living until our forties. And we do it because we want to help the world. What kind of crazy person would go for that?"—Nancy Andrews, Vice Chancellor for Academic Affairs and Dean of the Duke University School of Medicine

(Source)

3. Expanding humanity's knowledge
So the work environment is nice and lax, the pay is great, and your spouse certainly isn't rethinking their life decisions when it comes to marrying you.

But who needs those things?! We academics eschew time, family, and money for a higher purpose! We are adding to humanity's knowledge. One tiny (insignificant) nudge at a time:

(Source: Matt Might)

As long as you're fast enough:

(Source: Jorge Cham: PhD Comics)

4. Interacting with brilliant peers
Because in the end, pushing those insignificant boundaries of knowledge afford you the esteem of your peers. This, in turn, allows you to perpetuate the circle of scientific life!

Because someday, you too get to review scientific manuscripts and help build upon the foundations of progress.

* The writing and data presentation are so bad that I had to leave work and go home early and then spend time to wonder what life is about.
* This paper is desperate. Please reject it completely and then block the author’s email ID so they can’t use the online system in future.
* The biggest problem with this manuscript, which has nearly sucked the will to live out of me, is the terrible writing style.
* I suppose that I should be happy that I don’t have to spend a lot of time reviewing this dreadful paper; however I am depressed that people are performing such bad science.

(Source)

Enclosed is our latest version of Ms. #1996-02-22-RRRRR, that is the re-re-re-revised revision of our paper. Choke on it... Hopefully, we have suffered enough now to satisfy even you and the bloodthirsty reviewers...

To handle [the reviewers' suggestions], we have modified the Introduction and added, after the review of the relevant literature, a subsection entitled "Review of Irrelevant Literature" that discusses these articles and also duly addresses some of the more asinine suggestions from other reviewers.

We hope you will be pleased with this revision and will finally recognize how urgently deserving of publication this work is. If not, then you are an unscrupulous, depraved monster with no shred of human decency. You ought to be in a cage. May whatever heritage you come from be the butt of the next round of ethnic jokes. If you do accept it, however, we wish to thank you for your patience and wisdom throughout this process, and to express our appreciation for your scholarly insights.

(Source)

5. Educating young minds
But all of these awards pale in comparison to the cornerstone of academe: the student. As academics we are privileged with the highest of honors of educating tomorrow's thought-leaders!

One student complained that a professor was not posting lecture slides to the course’s Web site:
Is this a technical glitch, or are you being a jerk about it? I don’t think you know what your doing in this class. I have gone to the deprtment chair about it and she doesn’t know either. How can I study and take the exams without the notes? Its bad enough your lectures don’t have sound and video.

"I didn’t come to class today because i had a soar throat and couldn’t hear. I think it might be strep," the student wrote.
"Hello, Student X. I’m sorry you’re not feeling well. Did you intend to send this message to someone else? You’re not registered for any of my classes this semester. Oh, and I’m pretty sure that strep doesn’t cause loss of hearing," the professor replied.
"Ouch! i clicked the wrong address. can you forward that message to dr. DifferentProfessor for me? i can’t open the directory cuase my computer memory sucks and i have another program running. except change the hearing to talking. thanx!"

(Source 1 and 2)

(In all seriousness, despite these things, I really do love this job. "What kind of crazy person would go for that?" What kind of crazy person indeed.)

Cyranoski, D. (2011). Neuroscience in China: Growth factor Nature, 476 (7358), 22-24 DOI: 10.1038/476022a
Glass, R. (2000). A letter from the frustrated author of a journal paper Journal of Systems and Software, 54 (1) DOI: 10.1016/S0164-1212(00)00020-0
Lawrence, P. (2009). Real Lives and White Lies in the Funding of Scientific Research PLoS Biology, 7 (9) DOI: 10.1371/journal.pbio.1000197
Powell, K. (2006). Winning ways Nature, 442 (7104), 842-843 DOI: 10.1038/nj7104-842a

A New Model for Scientific Publishing

2011-12-26T08:39:00.000-08:00

There's a new paper out in Frontiers in Computational Neuroscience that is relavant to my interests. The paper is by Dwight Kravitz and Chris Baker from the NIMH and is titled "Toward a new model of scientific publishing: discussion and a proposal".

About two weeks ago Dwight emailed me his paper saying that he'd read a post I'd written last month for the Scientific American guest blog called "What is peer review for?" (you can check out my interview on Skeptically Speaking on this topic as well).

After reading Dwight's paper I want to make sure it gets as much exposure as possible. I can't it justice because it's so well-written and clear. But before I shuffle you off to read it I wanted to highlight their proposed system and ask you all what you think.

What are the barriers to instantiating their proposed system?

In the SciAm piece I concluded by saying:

But the current system of journals, editors who act as gatekeepers, one to three anonymous peer-reviewers, and so on is an outdated system built before technology provided better, more dynamic alternatives.

Why do scientists-–the heralds of exploration and new ideas in our society–-settle for such a sub-optimal system that is nearly 350 years old?

We can–-we should-–do better.

Well, it looks like Kravitz and Baker put a lot more thought into this problem than I and they've come up with an incredibly novel alternative system to peer review.

They nail it. There's almost nothing that I disagree with.

I love this paper.

They succeed here not because of their criticisms--which abound in the sciences--but rather because of their inclusion of a viable, creative, intelligent solution that addresses problems of motivation, utility, practicality, and even finance for an alternative model for peer review and scientific publication.

They begin by describing the current peer review system in the context of the neurosciences. They have an amusing graph that highlights the 17 levels of hell that is the peer review process loop. These guys crack me up.

"In the case of a rejection the Authors generally proceed to submit the paper to a different journal, beginning a journal loop bounded only by the number of journals available and the dignity of the Authors."

(click to enlarge)

Before I outline what their alternative proposal is, I want to highlight some of the problems regarding the costs and problems of the current system that Kravitz and Baker identify.

...what is striking is less the average amount of time [it takes to publish a paper], which is quite long, but more its unpredictability. In total, each paper was under review for an average of 122 days but with a minimum of 31 days and a maximum of 321. The average time between the first submission and acceptance, including time for revisions by the authors was 221 days (range: 31–533)...

...Beyond the costs of actually performing the research and preparing the first draft of the manuscript, it costs the field of neuroscience, and ultimately the funding agencies, approximately $4370 per paper and $9.2 million over the approximately 2100 neuroscience papers published last year. This excludes the substantial expense of the journal subscriptions required to actually read the research the field produces and the unquantifiable cost of the publishing lag (221 days) and the uncertainty incurred by that delay...

...Authors are incentivized to highlight the novelty of a result, often to the detriment of linking it with the previous literature or overarching theoretical frameworks. Worse still, the novelty constraint disincentives even performing incremental research or replications, as they cost just as much as running novel studies and will likely not be published in high-tier journals.

Okay, so what is their alternative model?

(click to enlarge)

It breaks down like this:

* No more editors as gate-keepers ("Their purpose is to serve the interests of the journal as a business and not the interests of Authors").
* Publication is guaranteed, so no more concern over "novelty".
* Editors instead coordinate the process and ensure that double-blind anonymity is maintained.
* Reviews are passed on to the authors as part of a "pre-reception" process which allows the authors to revise or retract their work before making it publicly available.
* Once public, the post-publication review process begins.
* An elected Editorial Board acts as an initial rating and classification service to put the paper in context.
* Members of the Board are financially incentivized... but the money doesn't go into their pockets, rather it can be put into their own research fund coffers.
* Papers are put into a forum wherein members of that forum can ask questions and offer follow-up suggestions.
* Forums provide a more living, dynamic quality to papers, as well as metrics for each manuscript.
* With better metadata for papers, ads could be more targeted by paper topic (no more ads for PCRs in cog neuro papers, for example).
* Kravitz and Baker note that something like a Facebook page for each paper could serve this purpose.

The Kravitz-Baker system saves money and time wasted by the needless "walking down the impact factor ladder" that usually occurs.

They address a lot more issues beyond what I've described above. They note that a common counter-argument to double-blind review, for example, is that a reviewer can "often guess" who the authors of the paper they're reviewing are because sub-fields are so small. But Kravitz and Baker point out that "the identity of the Authors might be guessed by the Reviewers, any ambiguity should act to reduce this bias". This seems so obvious.

The Kravitz-Baker system seems really well thought out, and one I'd love to see in place. But I'm worried I'm missing some critical fault here.

Anyone see any glaring issues?

Kravitz, D., & Baker, C. (2011). Toward a New Model of Scientific Publishing: Discussion and a Proposal Frontiers in Computational Neuroscience, 5 DOI: 10.3389/fncom.2011.00055

Am I a scientist?

2011-12-23T10:32:00.000-08:00

Over on Quora, someone asked me to answer the question "Am I a scientist?"

They gave the following details:

I am in the process of getting my PhD. I spend every day doing research. I "do" science. Can I put on my business card, "John Smith, Scientist"? Do I have to wait until I have the PhD in hand? Or until I'm a candidate?

I took a quick crack at it, but I'd love to hear what other people think. Here's my answer in full:

*****

There are two issues here: the first is one of credentials and the second is one of societal interpretation.

"Back off man..."

In the case of credentials, there is no exam, or class, or quiz, or whatever that one needs to pass in order to become a "scientist". There is no "science" credentialing system. Certainly if you are a PhD researcher working at a scientific research facility then you are a scientist. But so are all of that person's subordinates, who may or may not hold a PhD or even a degree at all!

Are Diederik Stapel and Marc Hauser still scientists? They hold PhDs and conducted research, but both were caught falsifying and/or fabricating data. That's certainly not scientific!

The second issue is one of societal interpretation. If you put on your business card "SCIENTIST", that gives the person reading the card the impression that you are currently a practicing researcher or theoretician. If you are not such, then you are being duplicitous and should not "advertise" yourself as a scientist. Not because you're not a scientist, but because you're sending a signal that isn't entirely true.

In your case, you are a PhD student. You are doing research (I presume); therefore you are a scientist.

That said, I believe you'd be better off putting "John Smith / Ph.D. candidate, awesomeology / University of Very Impressive" on your business card, as it is accurate, sends a signal that you're a "dedicated" scientist (i.e., working toward a PhD) and that all will carry the baggage of "being a scientist" for you, without the need to explicitly state it.

Now for my totally biased opinion: just calling yourself a "scientist" (without explicating what field of science you're specializing in) comes across as a little sleazy, like you're taking advantage of a title to pull one over on people. It's like people who constantly refer to themselves as "doctor"...

(image source from an older post of mine)

Feet, toes, penises, and brains

2011-12-08T08:32:00.000-08:00

Another answer to a Quora question. Best. Blog-fodder. Ever.

What might cause the split between people who think toes are ugly and toes are pretty?

People have different experiences that lead to different behaviors. But it's not like my past experience in thinking some women are ugly causes me to think all women are ugly. Why should that be the case for any aesthetic experience?

Thankfully the questioner gave me an out by asking what might cause some people to find toes pretty while others think they're ugly.

I'm going to use that to my advantage to give a completely unsubstantiated, just-so answer that's too cool for me to ignore. If more scientific evidence comes out on this topic I'll try to remember to adjust my answer accordingly.

Short answer: toes and penii might be closely related (neurologically speaking). For more science (SCIENCE!) read on.

In my answer to Why can't I control my individual toes? (two toe-neuroscience answers?! o_O I'm not even into toes!) I introduced the motor homunculus:

This guy's body parts are distorted such that the size of a body part is proportional to the area in the primary motor cortex that is dedicated to representing that part. This was first determined by Wilder Penfield by stimulating people's brains and mapping the motor responses of the body.

Just behind the primary motor cortex (blue in the figure below) is the primary somatosensory cortex (red). The somatosensory cortex is the final common pathway for all incoming touch sensations of the body (pain, light touch, etc.)

The representation here is similar the motor cortex and mirrors it quite closely. Save one pretty striking exception.

Meet the (male) somatosensory homunculus:

If you're up for it, here's the uncensored, possibly NOT WORK SAFE version (if your workplace hates science).

The first thing you'll notice is that the representation of our toes is much bigger on the somatosensory compared to the motor homunculus. (That was the first thing you noticed, right?) This means our toes are given a lot of brain area in the somatosensory cortex, which means we have relatively more sensitivity in our toes than, say, an equivalent area on our shins.

So lets take a look at the somatosensory map to see what the layout of body parts looks like on the brain:

Check out the locations of the toes there on the right. At the top, where the butt is, is the top of the brain. This image represents only one half of the brain, so the butt is actually at the top center, and right across from it, in the other half of the brain, the other half of your butt is represented.

This means that the toes are actually represented on the medial surface, squished between the two hemispheres of the brain (with each hemisphere having a representation of the toes on the opposite side of the body).

See what body part is represented right next to the toes, though!?

GENITALIA! Yay! I'm so close to actually answering the question now!

(See Why does the writing style of most PhDs on Quora appear to be long-winded and poorly structured?, bro.)

Here's the theory put forth by UCSD neuroscience rockstar VS Ramachandran:

In some people, neurons coding for or representing genetical sensation are "cross-wired" with neurons representing toes and feet. This cross-talk may give rise to the sexual associations of toes and feet.

This is far from proved, but it makes for a nice story. Ramachandran has done some clever experiments to test his theories about how neuronal "cross-wiring" gives rise to certain behavioral phenomena, such as synesthesia, so it's not a totally out-there hypothesis.

Ramachandran relates an amusing story of one of his patients about this topic:

The next day the phone rang again. This time it was an engineer from Arkansas.

"Is this Dr. Ramachandran?"

"Yes."

"You know, I read about your work in the newspaper, and it's really exciting. I lost my leg below the knee about two months ago but there's still something I don't understand. I'd like your advice."

"What's that?"

"Well, I feel a little embarrassed to tell you this."

"Doctor, every time I have sexual intercourse, I experience sensations in my phantom foot. How do you explain that? My doctor said it doesn't make sense."

"Look," I said. "One possibility is that the genitals are right next to the foot in the body's brain maps. Don't worry about it."

He laughed nervously. "All that's fine, doctor. But you still don't understand. You see, I actually experience my orgasm in my foot. And therefore it's much bigger than it used to be because it's no longer confined to my genitals."

It may be that neuroplasticity after this patient's limb loss induced communication between his foot and genital sensory neurons. This observation lends some support to Ramachandran's toe/brain/penis hypothesis.

For more on cool stuff related to neuroplasticity, see my answers to Can brain trauma cause cognitive enhancement? and When parts of the brain are removed during surgery, is it possible for the remaining brain tissue to expand into the available space?

For more reading on sex, brains, and homunculi, check out the neurocritic who's covered recent neuroscience research looking at the somatosensory representation of circumcised v uncircumcised male penises, the representation of the female homunculus, and the neuroscientific attempt to find the clitoris.

Hubbard EM, Brang D, & Ramachandran VS (2011). The cross-activation theory at 10. Journal of Neuropsychology, 5 (2), 152-77 PMID: 21923784

SciPle.org interview

2011-12-07T11:11:00.000-08:00

Lots of interviews this week!

Recently I presented some of the latest developments in my brainSCANr project at the Society for Neuroscience conference.

At my poster I was approached by SciPle.org, and Leonardo Restivo asked if I would do an interview with them. Well the interview's been posted and my answers are below. They're more personal than I was expecting, but I try not to shy away from personal questions (even if the answers can be uncomfortable).

Check Sci.Ple out; follow them on Twitter. They've got some really cool ideas that I'd love to see work out.

Sci.Ple: What is your background?
Technically I began my undergraduate career at the University of Southern California as a physics major. I grew up in San Diego with a lot of clear night skies. I wanted to be an astrophysicist. But that was not to be my path, and I ended up doing a degree in psychology while taking a host of philosophy and cognitive and computer science courses. I then worked as a research associate at UCLA for Edythe London; I was the PET scanner operator and radioactive pee cleaner (that's another story). In 2010 I completed my PhD in neuroscience at UC Berkeley under the mentorship of Robert Knight, the institute's director at the time. I'm currently a post-doctoral fellow at UCSF working with Adam Gazzaley.

Sci.Ple: Among your published papers, which one is your favorite?
Okay, I'm cheating a bit since it's not actually published yet, but it's close so I'm just going to act like it's published and hope that talking about it doesn't jinx the whole process. My favorite paper is one I co-wrote with my wife Jessica and is titled "Automated Cognome Construction and Semi-automated Hypothesis Generation". If I play by the rules of the question, then I'll go with "Hemicraniectomy: A new model for human electrophysiology with high spatio-temporal resolution" (Voytek et al., J Cogn Neurosci 2010).

Sci.Ple: Why is it your favorite?
Honestly I believe that the "Semi-automated Hypothesis Generation" paper is a Big Deal. We're text-mining the abstracts of millions of peer-reviewed neuroscience papers to try and make some sense out of how neuroscientific concepts interrelate. Then we're going one step further to see if we can find statistical "holes" in the literature… we're literally trying to (semi)automate one aspect of the scientific method: hypothesis generation.

Sci.Ple: What was the most challenging part of this paper?
The first spark of the idea for this paper came about during a panel I was on at a cognitive science conference in 2010. In response to a question from an audience member, I said something like, "the scientific literature is smarter than we are; many basic facts about brain function are probably already known, but we suck at synthesizing it all." Trying to prove that statement was the foundation for his paper. In order to write the paper I had to learn about text-mining, some graph theory, etc. It's totally outside of my comfort zone, but I think it's too cool to stress out about it not being "perfect".

Sci.Ple: What drives you in your day-to-day job?
Honestly? People literally pay to me to think about cool shit. That's my whole job. I get to say "I wonder if anyone has done this before," and then go out, run some experiments, and then possibly learn something that no one has ever known before. I've worked on a loading dock carrying heavy things onto trucks for up to 16 hours at a time. I've worked at a motel where my job was to go room to room and collect all of the... soiled... linens. So I guess the simplest answer to what drives me is a mix of awe and perspective. That's what keeps me going to work every day.

Sci.Ple: What is the most exciting part of your job?
Talking to other people. Collaborating and combining the accumulated knowledge of multiple brains in new ways to tackle hard problems. That's amazing. It's humbling and inspiring to see brilliant people's minds work.

Sci.Ple: The least exciting?
Paper formatting and data munging.

Sci.Ple: Name a scientist whose research inspires you
Reed Richards. That guy seems to be able to produce an endless stream of amazing, breakthrough ideas. Oh. Seriously? I've got a huge amount of respect for pre-digital scientists. Lots of them were going out and just trying everything. Sever the nerves in your own arm? Why not?! Cover yourself in varnish to prove that the skin does something important? Who cares if you almost died? You were right! I don't think I have the… fortitude… to do a lot of what those folks did--from the crazy self-experimentation to the drudgery of pre-digital writing and researching--I can't help but respect that.

Sci.Ple: What are the next frontiers in neuroscience?
Information integration. How do you go from a neuron giving off an action potential to a thought? From a neurotransmitter binding to a receptor to art? Imagine a Venn diagram that contains medicine, biology, genetics, psychology, philosophy, engineering, computer science, mathematics. That's neuroscience. Knowledge in each of these fields is being slowly accumulated (almost always separately) by doctors, biologists, geneticists, psychologists, philosophers, engineers, computer scientists, and mathematicians. We need more cross-disciplinary work.

Sci.Ple: Why science?
Why anything? My life, like almost everyone else's, has consisted of a series of half-blind stumbling steps. I got lucky. That said, I'll take the minor frustration of getting a paper rejected or having someone disagree with me over "soiled" towels and sheets any day.

Sci.Ple: If not science?
I'd work as a bartender at a pub. Or try and run my own. I love meeting and talking with people, and few places are better for than that a nice local watering hole.

Sci.Ple: Why?
"What happens to a werewolf on the moon?" I read that online the other day and it still cracks me up.

Skeptically Speaking radio interview

2011-12-04T08:46:00.000-08:00

Last month I wrote a piece about peer review for Scientific American.

Shortly thereafter I was contacted by Desiree Schell from the Skeptically Speaking radio show about doing a short interview on the topic. I love this podcast (it's one four I listen to after Science Friday, Radiolab, and TED talks), so I was pretty excited.

And--according to my wife--it was actually interesting. So yay to not being a boring knob. The interview starts with a discussion about faster than light neutrinos; I pop in around minute 43.

Here's the episode.

Anyway, if you haven't checked this show out, please do so. Their archives have great interviews with scientists and general science geeks such as Adam Savage, XKCD's Randall Munroe, and many others.

Is the female brain innately inferior?

2011-11-29T09:41:00.000-08:00

Did the title get your attention? It sure as hell caught mine when USC grad student Rohan Aurora sent me the link.

Recently Stanford's Clayman Institute for Gender Research published an interview with a Stanford neuroscientist about male vs. female brains.

I'm not going to lie: when I clicked the link I was expecting the usual attention-grabbing, rabble-rousing crap I've come to expect when I see a headline like that.

I was prepared for some serious eye rolling and frustrated groaning in response to the inevitable logical errors, overreaching conclusions, and other neuro-nonsense. Especially given how much gender has been on my mind lately (what with my recent foray into fatherhood and the whole #womanspace thing).

This certainly wouldn't have been the first time a neuroscientist has railed against silly neuroscientific claims in gender research.

Instead I got a well thought out, sane, clear-headed, and scientifically sound interview. I was especially pleased because the neuroscientist in question is a friend, colleague, and collaborator of mine: Prof. Josef Parvizi (co-author on one of my most-cited first-author papers). I'm especially proud to call him a collaborator after reading this. Seriously, this is a great interview and Josef just nails it.

The whole piece is short, but concise, and a great reference to counter some of the more common neuro-gender crap. They tackle three myths; I've quoted my favorite parts below.

Gender Brain Myth #1: Brain size matters

...if absolute brain size were all that mattered, whales and elephants, both of which have much larger brains than humans, would outwit men and women.

Gender Brain Myth #2: Women and men have different brains due to estrogen and testosterone

...if estrogen and testosterone did shape the brain in different ways, it is an unsubstantiated, logical leap to conclude that such differences cause, "...men to occupy top academic positions in the sciences and engineering or top positions of political or social power, while women are hopelessly ill-equipped for such offices."

Gender Brain Myth #3: Men are naturally better at math

According to Parvizi, this logic is flawed: "Differences seen in cognitive tests do not necessarily provide direct evidence that those differences are in fact innate."

Finally, I love the following. It should be copy-and-pasted into any online argument. Or shouted repeatedly at any TV/magazine puff-piece writer.

"...if we are to entertain the idea that humans 'experience' life differently, and that different experiences mold the brain function differently, then we must also seriously consider that gender (along with class, ethnicity, age, and many other factors) would also contribute to this experience, and that they will contribute to molding of the brain...

So if women and men have systematically different life experiences and face dissimilar expectations from birth, then we would expect that their brains would become different (even if they are not innately dissimilar), through these different life experiences. Even if neuroscientists see differences in the brains of grown men and women, it does not follow that these differences are innate and unchangeable.

For instance, if girls are expected to be more adept at language, and are placed in more situations that require communication with others, it follows that the networks of the brain associated with language could become more efficient in women. Conversely, if boys receive more toy trucks and Lego's, are given greater encouragement in math and engineering classes, and eventually take more STEM (science, technology, engineering and math) courses, it follows that the sections of the brain associated with mathematics could become more efficient in men...

The tricky part is that we do not make the mistake of taking account of these differences as evidence for biological determinism."

Ranking biomedical retractions

2011-11-18T08:24:00.000-08:00

This past week I was in Washington, DC for the 30,000+ Society for Neuroscience conference. Recently I wrote about (my interpretations of) the purpose of peer review. Well this prompted a group of us to get together to discuss open science and the future of scientific publishing.

Obviously science and the process of science have been on my mind.

My fellow neuroscientists Jason Snyder and Björn Brembs and I got together for lunch to talk about... lots of stuff, actually... but I came away with a few questions that seemed to have empirical answers.

Before I jump in though, if you haven't seen Björn's talk What's wrong with scholarly publishing today? check out the slides at the end of this post. They're packed with some mind boggling data about the business of peer-review.

At some point during our lunch, Retraction Watch (which is an amazing site), came up, and ultimately inspired two questions:

Which journals have the most retractions?
Which biomedical fields have the most retractions?

I did a quick-and-dirty check of this using PubMed's API, because they have a nice "search by retraction" option:

http://eutils.ncbi.nlm.nih.gov/entrez/eutils/esearch.fcgi?db=pubmed&field=word&term=hasretractionin&retmax=10000&usehistory=y

There was one issue: every article--regardless of scientific field--for the general science journals (Science, Nature, PNAS) are indexed in PubMed. So if an article (or a dozen) about semiconductors (see: Jan Hendrik Schön) was retracted from Science, it would still show up in this analysis. The result was inflated biomedical retraction counts for those journals, so I had to manually adjust counts down by removing non-biomedical retractions (just to put everything on par, since PubMed doesn't index non-biomedical peer-review journals).

Here are the results for the 1922 retractions across 796 journals:

PNAS (59 retractions) and Science (52) lead the pack, followed by J Biol Chem (40), J Immunol (33), and Nature (31).

Next I counted words that appeared in the titles of the retracted articles to get a feel for what kinds of papers are being retracted. Here's all words that appear at least 50 times in paper titles:

cells (189)
activity (154)
effects (152)
human (148)
patients (136)
protein (108)
factor (104)
gene (103)
expression (102)
receptor (96)
study (81)
cancer (70)
treatment (57)
surgery (54)
disease (54)
DNA (53)
virus (50)

(Similar words were grouped using TagCrowd)

At first blush, it looks like cell/molecular/micro biology represents a big chunk of the retractions (cells, protein, factor, gene, expression, receptor, DNA, virus), but human patient research isn't much better off... (human, patients, surgery).

I've heard the argument before (sorry, can't remember where) that fields where the data is more difficult to collect and replicate are more prone to shady research practices... I'm not sure if that's exactly being reflected here, but the exercise was an interesting one.

Thoughts?

What's wrong with scholarly publishing today? II

View more presentations from Björn Brembs

...the rest is just details

2011-11-12T16:33:00.000-08:00

(This cross-posted from my piece at Nature)

Meet the electric brain. A pinnacle of modern science! This marvel comes complete with a "centrencephalic system", eyes, ears, medial and lateral geniculate, corpora quadrigemina, and visual cortex.

(click to enlarge)

The text reads:

A giant electrified model of the human brain's control system is demonstrated by Dr. A.G. Macleod, at the meeting of the American Medical Association in New York, on June 26, 1961. The maze of twisting tubes and blinking lights traces the way the brain receives information and turns it into thought and then action.

It's a cheap journalistic trick to pull out a single example of hubris from the past at which to laugh and to highlight our own "progress". But where did the Electric Brain fail? Claims to understanding or modeling the brain have almost certainly been made countless times over the course of human thinking.

Hell, in moments of excitement with colleagues over a pint (or two) I've been known to shout, "I've figured out the brain!" But, of course, I have always been wrong.

So here we are, exactly 50 years post Electric Brain, and I find myself once again at the annual Society for Neuroscience conference (SfN). Each year we push back the curtain of ignorance and, just as I have every year since I began my neuroscience career in 2003, I find myself surrounded by 30-40,000 fellow brain nerds.

How do the latest and greatest theories and findings on display at SfN compare to the Electric Brain? One would like to think that, with this much brain power (har, har), surely we must be close to "understanding the brain" (whatever that might mean). Although any model of the human brain feels like an act of hubris, what good are countless scientific facts without an integrated model or framework in which to test them?

The Electric Brain is an example of a connectionist model in which the brain is composed of a collection of connected, communicating units. Thus, the brain can be modeled by the interconnections between all the subregions of it; behavior is thought to be an emergent property of the complexities of these interconnected networks of units.

A "unit" in the Electric Brain appears to be a whole region, whose computations are presumably modeled by a simple input/output function. The modern incarnations of this movement are seen in the rapidly maturing field with the sexy name of connectomics, the underlying belief of which is that if we could model how every neuron connects to every other neuron, we would understand the brain.

With advancements in computational power, we've moved beyond simplified models of entire brain regions and toward attempts to model whole neurons, such as this model of 10^11 neurons by Izhikevich and Edelman (Large-Scale Model of Mammalian Thalamocortical Systems, PNAS 2008).

There are also attempts to model the brain at the molecular level, such as with the Blue Brain Project.

But as Stephen Larson, a PhD candidate at UCSD astutely noted on Quora,

To give you a sense of the challenge here, consider the case of a simple organism with 302 neurons, the C. elegans. There has been a published connectome available since 1986... however, there is still no working model of that connectome that explains the behavior of the C. elegans.

One issue with this approach is that the brain is dynamic, and it is from this dynamism that behavior arises (and the complexities of which are hidden in a static wiring diagram). Wilder Penfield summed it up nicely, "Consciousness exists only in association with the passage of impulses through ever changing circuits of the brainstem and cortex. One cannot say that consciousness is here or there" (Wilder Penfield: his legacy to neurology. The centrencephalic system, Can Med Assoc J 1977).

In my most cynical moments, connectionist approaches feel like cargo cult thinking, whereby aping the general structure will give rise to the behavior of interest. But how can we learn anything without first understanding the neuroanatomy? After all, our anatomy determines the rules by which we are biologically constrained.

This year I spoke at the 3rd International Workshop on Advances in Electrocorticography. Across two days there were a total of 23 lectures on cutting-edge methods in human and animal electrophysiology. Last year I attended a day-long, pre-SfN workshop titled "Analysis and Function of Large-Scale Brain Networks".

During both of these sessions I sometimes found it difficult to restrain my optimism and enthusiasm (yes, even after all these years "in the trenches"). And while wandering through a Kinko's goldmine of posters and caffeinating myself through a series of lectures, occasionally I forget my skepticism and cynicism and think, "wow, they're really on to something."

And that's what I love about this conference: every year it gives me a respite from cynicism and skepticism to see so many scientists who are so passionate about their work. Sure, it might be hubris to think that we can model a brain, but so what? When the models fail, scientists will learn, the field will iterate, and the process will advance.

That's what we do, and that's why I keep coming back. The Society for Neuroscience conference is my nerd Disneyland.

Izhikevich EM, & Edelman GM (2008). Large-scale model of mammalian thalamocortical systems. Proceedings of the National Academy of Sciences of the United States of America, 105 (9), 3593-8 PMID: 18292226
Jasper HH (1977). Wilder Penfield: his legacy to neurology. The centrencephalic system. Canadian Medical Association journal, 116 (12), 1371-2 PMID: 324600

What is peer-review for?

2011-11-02T07:42:00.000-07:00

(This is re-posted from the Scientific American Guest Blog)

There is a lot of back and forth right now amongst the academic technorati about the "future of peer review". The more I read about this, the more I've begun to step back and ask, in all seriousness:

What is scientific peer-review for?

This is, I believe, a damn important question to have answered. To put my money where my mouth is I'm going to answer my own question, in my own words:

The scientific peer-review process increases the probability that the scientific literature converges--at long time scales--upon scientific truth via distributed fact-checking, replication, and validation by other scientists. Peer review publication gives the scientific process "memory".

(Cover of the first scientific journal, Philosophical Transactions of the Royal Society, 1665-1666. Source: Wikipedia)

Note that publication of methods and results in a manner that they can be peer-reviewed is a critical component here. Given that, let's take part in a hypothetical regarding my field (neuroscience) for a moment.

In some far-distant future where humanity has learned every detail there is to know about the brain, what does the scientific literature look like in that world? Is it scattered across millions of closed, pay-walled, static manuscripts as much of it is now? Does such a system maximize truth-seeking?

And, given such a system, who is the megamind that manages to read through all of those biased (or incomplete, or incorrect) individual interpretations to extract the scientific truths to distill a correct model of the human brain and behavior (whatever that might entail)?

I am hard-pressed to imagine that this future scientific literature looks like what we currently possess. In fact, there are many data-mining efforts underway designed to overcome some of the limitations introduced by the current system (such as, for cognitive neuroscience, NeuroSynth and my own brainSCANr).

The peer-review system we have now is incomplete.

I'm not attacking peer-review, I'm attacking peer-review based on journal editors hand-picking one to three scientists who then read a biased presentation of the data without being given the actual data used to generate the conclusions. Note that although I am only a post-doc, I am not unfamiliar with the peer-review process, as I have "a healthy publication record" and have acted as reviewer for a dozen "top journals".

To gain a better perspective, I read this peer-review debate published in Nature in 2006.

In it, there were two articles of particular interest, titled:

* What is it for?
* The true purpose of peer review

These articles, in my opinion, are lacking answers to the questions that are their titles.

Main points from the first article:

* "For authors and funding organizations, peer review provides an important veneer of respectability."
* "For editors, peer review can help inform the decision-making process... Prestigious journals base their reputation on their exclusivity, and take a 'top-down' approach, creaming off a tiny proportion of the articles they receive."
* "For readers with limited time, peer review can act as a filter, reducing the amount they think they ought to read to stay abreast."

The first two points are issues of reputation management, which ideally have nothing to do with actual science (note, I say ideally...) The second point presupposes that publishing results in journals is somehow the critical component, rather than the experiments, methods, and results themselves. The final point may have been more important before the advent of digital databases, but text-based searches lessens its impact.

Notably, none of these mention anything about science, fact-finding, or statements about converging upon truth. (Note, in the past I've gone so far as to suggest that even the process of citing specific papers is biased and flawed, and that we would be better off giving aggregate citations of whole swathes of the literature.)

The second article takes almost an entirely economic, cost-benefit perspective of peer-review again focused on publishing results in journals. Only toward the end does the author directly address peer-review's purpose in science by saying:

...[T]he most important question is how accurately the peer review system predicts the longer-term judgments of the scientific community... A tentative answer to this last question is suggested by a pilot study carried out by my former colleagues at Nature Neuroscience, who examined the assessments produced by Faculty of 1000 (F1000), a website that seeks to identify and rank interesting papers based on the votes of handpicked expert 'faculty members'. For a sample of 2,500 neuroscience papers listed on F1000, there was a strong correlation between the paper's F1000 factor and the impact factor of the journal in which it appeared. This finding, albeit preliminary, should give pause to anyone who believes that the current peer review system is fundamentally flawed or that a more distributed method of assessment would give different results.

I strongly disagree with his final conclusion here. A perfectly plausible explanation for this result would be that scientists rate papers in "better" journals higher because they're published in journal perceived to be better. This would appear to be a source of bias and a major flaw of the current peer-review system. Rather than giving me pause as to whether the system is flawed, one could easily interpret that result as proof of the flaw.

The most common response that I encounter when speaking with others scientists about what they think peer-review is for, however, is some form of the following:

Peer-review improves the quality of published papers.

I'm about to get very meta here, but post-doc astronomer Sarah Kendrew recently wrote a piece in The Guardian titled, "Brian Cox is wrong: blogging your research is not a recipe for disaster".

This was followed by a counter post in Wired by Brian Romans titled "Why I Won’t Blog Unpublished Results". In that piece, Brian also says that peer-review improves papers:

First of all, the formal peer-review process has definitely improved my submitted papers. Reviewers and associate editors can catch errors that elude even a team of co-authors. Sometimes these are relatively minor issues, in other cases it may be a significant oversight. Reviewers typically offer constructive commentary about the formulation of the scientific argument, the presentation of the data and results, and, importantly, the significance of the conclusions within the context of that particular journal. Sure, I might not agree with every single comment from all three or four reviewers but, collectively, the review improves the science. Some might respond with ‘Why can’t we do this on blogs! Wouldn’t that be great! Internets FTW!.’ Perhaps someday. For now, it’s difficult to imagine deep and thorough reviews in the comment thread of a blog.

(emphases mine)

Although Brian concedes (but dismisses) the fact that none of these aspects of peer-review need be done in formal journals, he argues that because his field doesn't use arXiv and there is currently no equivalent for it, then journals are still necessary.

We also see an argument in there about how reviewers guide statements of significance for a particular journal, and the conclusion that somehow these things "improve the science". But even the narrative that peer-review improves papers can be called into question:

Smith R. Peer review: a flawed process at the heart of science and journals. J R Soc Med, 99(4); 2006

Another answer to the question of what is peer review for is that it is to improve the quality of papers published or research proposals that are funded. The systematic review found little evidence to support this, but again such studies are hampered by the lack of an agreed definition of a good study or a good research proposal.

Rothwell PM and Martyn CN. Reproducibility of peer review in clinical neuroscience. Brain, 123(9); 2000

Peer review is central to the process of modern science. It influences which projects get funded and where research is published. Although there is evidence that peer review improves the quality of reporting of the results of research, it is susceptible to several biases, and some have argued that it actually inhibits the dissemination of new ideas.

To reiterate: peer-review should be to maximize the probability that we converge on scientific truths.

This need not happen in journals, nor even require a "paper" that needs improvement by reviewers. Papers are static snapshots of one researcher or research teams' views and interpretations of the results of their experiments.

Why are we even working from these static documents anyway?

Why--if I want to replicate or advance an experiment--should I not have access to the original data and analysis code off which to build? These two changes would drastically speed up the scientific process. Almost any argument against implementing a more dynamic system seems to return to "credit" or "reputation". To be trite about it, if everyone has access to everything, however will they know how clever I am? Some day I expect a Nobel Prize for my cleverness!

But a "Github for Science" would alleviate even these issues. Version tracking would allow ideas to be traced back to the idea's originator with citations inherently built into the system.

I'm not saying publishing papers is bad. Synthesis of ideas allows us to publicly establish hypotheses for other scientists to attempt to disprove. But most results that are published are minor extensions of current understanding that don't merit long-form manuscripts.

But the current system of journals, editors who act as gatekeepers, one to three anonymous peer-reviewers, and so on is an outdated system built before technology provided better, more dynamic alternatives.

Why do scientists--the heralds of exploration and new ideas in our society--settle for such a sub-optimal system that is nearly 350 years old?

We can--we should--do better.

Wager, E. (2006). What is it for? Analysing the purpose of peer review. Nature DOI: 10.1038/nature04990
Jennings, C. (2006). Quality and value: The true purpose of peer review Nature DOI: 10.1038/nature05032
Editors (2005). Revolutionizing peer review? Nature Neuroscience, 8 (4), 397-397 DOI: 10.1038/nn0405-397
Smith, R. (2006). Peer review: a flawed process at the heart of science and journals Journal of the Royal Society of Medicine, 99 (4), 178-182 DOI: 10.1258/jrsm.99.4.178
Rothwell, P. (2000). Reproducibility of peer review in clinical neuroscience: Is agreement between reviewers any greater than would be expected by chance alone? Brain, 123 (9), 1964-1969 DOI: 10.1093/brain/123.9.1964

The Zombie Brain: Conclusions

2011-10-31T08:09:00.000-07:00

This post is the final installment of our collaborative venture on exploring the Zombie Brain. We hope you’ve enjoyed the ride.

Sincerely, Bradley Voytek Ph.D. & Tim Verstynen Ph.D.

Bringing it all together: The Zombie Brain

Over the last ten days we’ve laid out our vision of the Zombie Brain. To recap, we’ve shown that zombies:

1) Have an over-active aggression circuit
2) Show cerebellar dysfunction
3) Suffer from long-term memory loss due to damage to the hippocampus
4) Present with global aphasia (i.e., can’t speak, can understand language)
5) Suffer from a variant of Capgras-Delusion
6) Have impaired pain perception
7) Cannot attend to more than one thing at a time
8) Exhibit addictive responses to eating flesh
9) Have an insatiable appetite

Together, these symptoms and their neurological roots reveal a striking picture of the zombie brain.

Based on the behavioral profile of the standard zombie, we conclude that the zombie brain would have massive atrophy of the “association areas” of the brain: i.e., those areas that are responsible for the higher-order cognitive functions. Given the clear cognitive and memory deficits, we would also expect significant portions of the frontal and parietal lobes, and nearly the entire temporal lobe, to exhibit massive degeneration. As such, the hippocampuses of both hemispheres would be massively atrophied (resulting in memory deficits), along with most of the cerebellum (resulting in a loss of coordinated movements).

In contrast, we would expect that large portions of the primary cortices would remain intact. Behavioral observations lead us to conclude that vision, most of somatosensation (i.e., touch), and hearing are likely unimpaired. We also hypothesize that gustation and olfaction would also remain largely unaffected. We must further conclude that large sections of the thalamus and midbrain, brainstem, and spinal cord are all likely functioning normally or are in a hyper-active state.

Putting these elements together, we have reconstructed a plausible model for what the zombie brain would look like.

Overlay (yellow is zombie, gray is human)

It is interesting to point out, from an historical standpoint, that many of the regions we hypothesize to be damaged in the zombie brain are part of what is generally referred to as the Papez circuit. James Papez first identified this circuit in 1936. Much like our current study, Papez was trying to unify a cluster of behavioral phenomena he had observed into a neuroanatomical model of the brain. He wondered why emotion and memory are so strongly linked. Thus, he hypothesized that emotional and memory brain regions must be tightly interconnected.

To test this theory, he injected the rabies virus into the brains of cats to watch how it spread and he made note of which brain regions were destroyed as a result of these injections. He observed that the hippocampus (important for memory formation) connects to the orbitofrontal cortex (social cognition and self-control), the hypothalamus (hunger regulation, among other things), the amygdala (emotional regulation), and so on. These experiments, conducted almost three-quarters of a century ago, may shed some insight into the nature of the zombie disorder today. We’re not suggesting that some super, brain-eating rabies virus is responsible for zombies. We’re just saying that it’s not not possible.

The profile of damage we have outlined corroborates the behavioral observations we have made from zombie films. From a subjective standpoint, this pattern of cerebral atrophy represents a most heinous form of injury unparalleled in the scientific literature. It would lead to a pattern of violence and social apathy; patients thus affected would represent a grievous harm to society, with little chance of rehabilitation. The only recommendation is immediate quarantine and isolation of the subject.

However, as we learned in GI Joe “knowing is half the battle.” Based on our observations, we leave you with a few strategies to maximize survival in the event of a zombie encounter.

1) Outrun them: Climb to a high point or some other place they will have trouble reaching. Practice parkour. The slow zombie variant can’t catch up with a healthy adult human.

2) Don’t fight them: They can’t feel pain and aren’t afraid of dying, so they’ve got the edge in close combat. If you can simply out run them, why risk the bite?

3) Keep quiet and wait: The zombie memory is so terrible that if you can hide long enough, it will mill around only until something else captures its attention.

4) Distraction, distraction, distraction: Throw something behind the zombie to capture its attention. Set off a flare, use a flashbang, or whatever you need to do to distract it to get away

5) If you can’t beat ‘me, join ‘em: If you can’t out run them (or are around the fast zombie variant) take advantage of their self-other delusion and act like one of them.

There you have it folks... scientifically validated safety tips for surviving the zombie apocalypse. Use them wisely the next time you come face-to-face with the living dead.

The Zombie Brain: Insatiable Hunger

2011-10-30T09:00:00.000-07:00

This is the last symptom of the multi-day series on The Zombie Brain between Oscillatory Thoughts and The Cognitive Axon.

Be sure to check out our last post tomorrow in which we wrap everything up.

Symptom 9: Insatiable Hunger

What drives the zombie’s insatiable hunger for human flesh? In the last post we discussed the role of addiction in the zombie’s craving for your skin, but why are they never satisfied? Why, after having eating your entire family, will the zombie continue on to consume you as well? How can they keep eating?

While we cannot ascertain for certain the etiology of zombie hunger, we posit two possible neural mechanisms that underlie this disorder.

First and most probable is the alteration of the hunger/satiety circuit in the zombie brain. In a previous post we outlined the nature of the zombie impulsive-reactive aggression. In that post we demonstrated that damage to the zombie orbitofrontal cortex would lead to alterations in the top-down control over subcortical nuclei such as the hypothalamus.

The hypothalamus plays an important role in maintaining control over autonomic functions such as regulating body temperature and the sleep/wake cycle, as well as modulating thirst and hunger. Dysfunction of this region due to abnormal activity--either from the loss of or damage to connecting regions, or possibly via unknown neurochemical changes--would severely affect zombie satiety and sleep.

For example, we are often taught that the ventromedial nucleus of the hypothalamus regulates feelings of satiety while the lateral nucleus regulates feeding (quick mnemonic: "stim the ven, get thin; stim the lat, get fat"). Thus, damage to the zombie ventromedial nucleus may result in a loss of satiety.

In other words: zombies will always be hungry. For you.

(Though, as with all things neuroscience, this may be more complicated than we are taught.)

The second possible mechanism for zombie fleshlust may be the result of a form of Klüver–Bucy syndrome.

This interesting disorder is caused by damage to both temporal lobes and is associated with an array of disorders including hyperphagia (overeating) as well as pica (eating strange objects).

Sound familiar? I would say eating flesh would constitute as eating a "strange object".

This is a very rare disorder that usually only occurs in experimental settings where researchers intentionally remove the temporal lobes of an animal. However, it is also associated with other symptoms including placidity, emotional dysregulation, and hypersexuality. See exhibit A below (from the Annals of Mad Science, circa 1930):

So while Klüver–Bucy would account for the eating patterns seen in zombies, few would associate placidity or sexuality with the walking dead.

In fact, hyperorality, pica, hypersexuality, and strange emotional responses sound more like symptoms of sparklevampires.

And insatiable hunger is also associated with other Awesome Beings, so these phenomena may underlie the abnormal behavioral patterns observed in other, more rare, non-zombie subjects...

King BM (2006). The rise, fall, and resurrection of the ventromedial hypothalamus in the regulation of feeding behavior and body weight. Physiology & behavior, 87 (2), 221-44 PMID: 16412483

Zombie Brain: Flesh addiction

2011-10-29T09:55:00.000-07:00

Head over to The Cognitive Axon for our eighth symptom of zombie brain and behavior: flesh addiction!

The Zombie Brain: Stimulus-locked Attention

2011-10-28T09:00:00.000-07:00

This is part eight(!) of our multi-day series on The Zombie Brain.

Be sure to visit The Cognitive Axon tomorrow for symptom 8!

Symptom 7: Stimulus-locked attention

If zombies are anything, they're at least highly distractible. Don't want them to see that you're looting an old corner store for supplies? Throw up a few fireworks. The walking dead will be occupied as long as the show lasts.

Of course, this type of attention can be deadly if the critters set their sights on you...

This type of stimulus-bound attention reflects another rare clinical disorder called simultanagnosia. Simultanagnosia, particularly the "dorsal form", is the inability to attend to more than one thing at time and is often seen in patients suffering from Balint's Syndrome.

The only thing these patients perceive is whatever has grabbed their attention. This originates when both the left and right parietal cortex, the back and top part of your neocortex, are lesioned. If one is intact, spatial attention is still somewhat impaired, but the impenetrable stimulus-locking does not occur.

Damage to this parietal network may also underlie some of the issues we previously described with the mirror neuron network, language regions, and pain sensory regions.

So, along with a good chunk of the frontal lobe, it's safe to assume that the dorsal parietal lobe is lesioned in the zombie brain as well. This could happen if the neurons themselves are destroyed, or if the axons connecting them (called "callosal fibers" because they pass through the corpus callosum) are damaged.

Only careful, clinical trials can tell us the true root cause of this damage in the zombie brain. Nevertheless, by arming ourselves with the knowledge of the zombie’s simultanagnosia, we can devise further survival strategies. More on this later.

The Zombie Brain: Bring the pain!

2011-10-27T10:18:00.000-07:00

Head over to The Cognitive Axon for our sixth symptom of zombie brain and behavior: pain perception!!

The Zombie Brain: Self/Other Delusion

2011-10-26T09:00:00.000-07:00

This is part six of our multi-day series on The Zombie Brain.

Be sure to visit The Cognitive Axon tomorrow for symptom 6!

Symptom 5: Self/Other Delusion

So what exactly did we do to piss off the living dead? Oh sure, you probably had a grudge or two with someone who's risen from the grave, but most of the walkers coming after you have no idea who you are.

Zombies are just plain delusional; they see us as something else, something they can't make sense of. While modern neuroscience is still just beginning to understand the neural underpinnings of delusional disorders, this particular type of self/other association delusion has been linked at least two distinct circuits in the brain.

First, the inability for a zombie to recognize that they're chowing down on their bowling partner mirrors a very rare neurological disorder called the Capgras delusion.

Individuals with Capgras are convinced that the people they know well (e.g., a close friend or spouse) have been replaced by an imposter. It's like an alien came down and replaced your teammate with a lookalike that wasn't him. Think Invasion of the Body Snatchers.

Now we don't know precisely what causes the Capgras delusion, but let's suffice it to say that the zombie brain most likely has it! One hypothesis is that the brain regions that recognize faces (the fusiform face area) and the regions that assign emotional content to experience (the amygdala), which are normally communicating nicely, are somehow disrupted.

You can see Ramachandran talk about it on this TED video:

This means that people with Capgras can still recognize people as people but that they don't have any emotional ties to them. Couple that with the orbitofrontal aggression and control issues we described earlier, and you could see how this would get out of hand!

Therefore, the zombie is after you not only because they're pissed off and looking for a food source, but because they literally don't recognize you as the person they once loved.

Second, this ability to recognize "self" from "other" may also reflected in a set of frontal and parietal neurons called mirror neurons. These cells turn on when you perform an action (say picking up an ax) and when you see someone else perform the same action.

Some scientists believe that mirror neurons play an intimate role in social bonding and empathy; both behaviors that zombies clearly lack. Now, some have said that zombies completely lack mirror neurons altogether. However, that doesn't seem reasonable since zombies tend to imitate what they see (particularly things other zombies do).

Likely, the response properties of these cells have changed. If you were to stick an electrode in a zombie's inferior frontal cortex, you’d likely observe mirror neurons that only respond when a zombie performs an action or sees another zombie performing the same action.

Both brain dysfunctions point out one key survival skill: if you want a zombie to not come after you... start acting like a zombie. They'll think you’re one of them and might even follow you into a well-devised trap. This demonstrates that, by understanding the neural basis of the zombie disorder, we can begin building protocols that will maximize our survival.

Zombie Brain: Language deficits

2011-10-25T09:54:00.000-07:00

Head over to The Cognitive Axon for our fourth symptom of zombie brain and behavior: language issues!

The Zombie Brain: Long-term Memory Loss

2011-10-24T09:00:00.000-07:00

This is part four of our multi-day series on The Zombie Brain.

Be sure to visit The Cognitive Axon tomorrow for symptom 4!

Symptom 3: Long term memory loss

Why is it that it only takes you a few seconds to hide from zombies before they get distracted, forget their prey, and move on after some other helpless chap? Yet they flock in droves to places like malls and churches that they remember from their pre-zombie past?

We contend that zombies are incapable of storing long-term memories as a result of a disorder called anterograde amnesia. Anyone who's seen the movie Momento will know the symptoms well. Immediate events are available for only a few minutes at a time, at most, before their flow of conscious memories is disrupted.

Once distracted, someone afflicted with anterograde amnesia will lose those memories as if they never existed at all. However, memories that were gained before the amnesia-inducing brain damage will be retained as clearly as if they had happened yesterday.

This phenomenon arises from damage to a very specific area of the brain called the hippocampus. This region sits right behind the amygdala (which we talked about earlier) and is nestled deep within the temporal lobe. For such severe amnestic symptoms, our hypothetical zombie subjects would have to lose both their left and right hippocampuses.

This is a rare condition that has so far really only come about for surgical reasons and doesn't really tend to happen naturally. However, there are cases in which severe vitamin deficiency can lead to memory issues and anterograde amnesia. This is due to the susceptibility of the mamillary bodies, a brain region that is heavily interconnected with the hippocampus, to vitamin deficiency degeneration.

This leads to a disorder referred to as Wernicke-Korsakoff’s syndrome, characterized by memory disruptions, which may be involved in regulation of the hippocampus. Whether a virus has destroyed the hippocampus, or zombies are simply suffering from a severe vitamin deficiency, it's safe to say that somehow they've lost their hippocampuses for good, as well as any ability to form memories of the new un-life.

Zombie Brain: Lumbering Walk

2011-10-23T09:51:00.000-07:00

Head over to The Cognitive Axon for our second symptom of zombie brain and behavior: their lumbering walk!

The Zombie Brain: Impulsive-Reactive Aggression

2011-10-22T09:00:00.000-07:00

This is part two of our multi-day series on The Zombie Brain.

Be sure to visit The Cognitive Axon tomorrow for symptom 2!

Symptom 1: Impulsive-reactive aggression

It’s pretty much a given that zombies are constantly pissed off and they want to eat you. The snarls, the teeth, the guttural howls as they close in on their prey... these creatures are enough of a public health danger and menace to warrant serious research funding from the National Institutes of Health!

The adrenalin-infused rage of thousands of raging beasts is unmistakable.

So what does this uncontrolled, rampant rage tell us about the zombie brain? First, the type of rage that zombies exhibit is of a very primal form known as impulsive-reactive aggression. This is more like the aggression you see when two drunks get in a fight.

It differs from the cold and calculated rage seen, for example, in a school shooting. The zombies will direct their anger at anyone and everyone simply because they're human. This type of rage has its roots in the more “primitive” (i.e., phylogenetically older) parts of the brain and reflects the engagement of the “fight-or-flight” circuitry that all mammals have. Steve Schlozman has referred to this circuit as the "crocodile brain".

Normally, these every-day anger impulses are suppressed by signals that originate in the lower part of the frontal lobe: the orbitofrontal cortex. This area sends inhibitory signals to the medial amygdala, a little almond-shaped area that sits at the front of your temporal lobe. If left uncontrolled this tiny region would ramp up signals to the hypothalamus and thalamus that trigger the adrenal responses you feel when angry and frightened. But since most of us have an intact orbitofrontal cortex, the little amygdala is turned down except in rare cases.

Studies of violent, pathological criminals have found that functional abnormalities of the dorsal and ventral prefrontal cortices and the amygdala may underlie some anti-social and violent behaviors. Furthermore, people with damage to the orbitofrontal cortex often have issues with social cognition, understanding and adhering to social norms and mores, as well as moral decision-making.

Some of you may have heard of the famous case of Phineas Gage who had a rod shot through his brain and went from mild-mannered middle management to uninhibited risk-taker and speaker of all things inappropriate. Well that’s because he lost his orbitofrontal cortex.

Certainly the zombie doesn’t care about social norms or morality!

Given the impulsive and aggressive behavior exhibited by zombies, it’s safe to say that they
lack a properly functioning orbitofrontal cortex. So we’ve modeled the zombie brain such that the orbitofrontal cortex is more or less obliterated. As a result, the zombie amygdala, hypothalamus, and thalamus (specifically the bed nuclei of the stria terminalis) should be constantly overactive. These changes would easily produce a hair-trigger adrenal response unlike anything seen in normal humans!

The Zombie Brain

2011-10-21T09:00:00.000-07:00

The Living Dead Brain: What Forensic Neuroscience Can Tell Us about the Zombie Brain
Dr. Timothy Verstynen & Dr. Bradley Voytek
Zombie Research Society

This is a cross-post between Oscillatory Thoughts and Cognitive Axon. Stay tuned to both sites over the following days leading up to Halloween for updates on our model of the zombie brain.

What can neuroscience teach us about surviving the zombie apocalypse?

What makes a zombie a zombie or, more importantly, what makes a zombie not a human? Philosophers contend that a zombie lacks that qualia of experience that belies normal consciousness.

However this is a less than satisfying explanation for why the lumbering, flesh eating creatures are pounding outside the door of your country farmhouse.

Beyond the (currently) immeasurable idea of consciousness or the whole supernatural “living dead” theory, zombies are characterized primarily by their highly abnormal but stereotyped behaviors. This is particularly true in more modern manifestations of the zombie genre wherein zombies are portrayed not as the reanimated dead, but rather as living humans infected by biological pathogens. They are alive, but they are certainly not like us.

Neuroscience has shown that all thoughts and behaviors are associated with neural activity within the brain. Therefore, it should not be surprising that the zombie brain would look and function differently than the gray matter contained in your skull. Yet, how would one know what a zombie brain looks like?

Luckily, the rich repertoire of behavioral symptoms shown in cinema gives the astute neuroscientist or neurologist clues as to the anatomical and physiological underpinnings of zombie behavior. By taking a forensic neuroscience approach, we can piece together a hypothetical picture of the zombie brain.

Over the course of the next week, Oscillatory Thoughts and Cognitive Axon will team up to show our hypothetical model of the zombie brain. Each day we will present a new "symptom" associated with a zombie behavior and show its neural correlates in our simulated zombie brain.

This entire endeavor is partly an academic "what if" exercise for us and partly a tongue-in-cheek critique of the methods of our profession of cognitive neuroscience. We’ll be breaking up the workload and alternating days (hey... we gotta work our real jobs too) so be sure to check both places for the newest updates on zombie neuroscience.

DISCLAIMER: We need to be very clear on one point. While we sometimes compare certain symptoms in zombies to real neurological patient populations, we are in no way implying that patients with these other disorders are in some way “part zombie”. Neurological disorders have provided critical insights into how the brain gives rise to behavior and we bring them up for the sake of illustration only. Their reference in this context is in no way meant to diminish the devastating impact that neurological diseases can have on patients and their caregivers.

Forbes "Edge Thinkers"

2011-10-19T08:18:00.000-07:00

On Monday my interview with Forbes went live:

Neuroscientist Bradley Voytek is Bringing the Silicon Valley Ethos into Academia

This was part of their "Working The Edge" series.

Recently Forbes managing editor Bruce Upbin put out a call for "Edge Thinkers":

Forbes just launched a new section on our Tech channel to showcase intriguing people operating at the fringes of science, business, education, government, healthcare and the arts. It’s called Working The Edge. It’s a way to cover the kinds of people who innovate by merging seemingly unrelated disciplines. The kinds of people with three degrees, or else are entirely self-taught. They are the associative thinkers mixing biology and architecture, chemistry and marketing, charity and capitalism, Shakespeare and data mining, and food and physics. They’re not superheroes or brainiacs, just ordinary people who work hard and passionately at exploring a big new idea. Okay, sometimes they’re brainiacs.

Last week I got an email from Forbes writer Alex Knapp (who writes the Robot Overlords blog) saying that my name was on their list.

A few days later we did an hour-long phone interview.

We talked about zombies (of course), Uber and my "startup sabbatical", my TEDxBerkeley talk about my grandfather's Parkinsonism, brainSCANr, my PhD research, and how my wife can kick my ass at writing code.

It was a lot of fun (though it did hit some of my "what the hell am I doing?" anxiety buttons) and, I think, a good interview.

So yeah, check it out.

Why you can't individually control your toes

2011-10-17T07:12:00.000-07:00

Man, Quora's becoming a great resource for my blog. It keeps giving me amusing ideas to write about.

Recently someone asked "Why can't I control my individual toes?".

This was a really fun answer to write, so I thought I'd share it here.

*****

Before explaining this, I want you to try a quick experiment for me: hold your hand in front of you, fingers straight and pointing upward. Now, flex your index finger and just your index finger. Did your middle finger flex, too? Maybe your ring finger even twitched a little? Try flexing just your ring finger. Unless you're a piano or string instrument player, it's unlikely that you were very successful at doing so.

The reason why that happens is closely related to why you can't control your individual toes. Stick with me.

This sexy beast is the motor homunculus:

He's built to reflect the relative area in the motor cortex that is devoted to controlling specific muscle groups. Notice how overrepresented the hands, lips, and eyes are and how underrepresented the arms, legs, and feet are?

Here's the motor cortex in the brain:

Basically, the more motor cortical area devoted to a region, the greater and finer the voluntary control over those muscles groups that we have.

Originally this map was created by Canadian neurosurgeon Wilder Penfield in 1937. Penfield pioneered brain surgery on awake patients. He would use a small electrical stimulator to map out different parts of the brain, which is still done by neurosurgeons to this day. The logic was simple: stimulate a part of the motor cortex and watch which parts of the body twitched. This gives a mapping between brain and body, and what he found was a clear topography in the motor cortex.

Journalist and science writer Mo Costandi wrote an amazing history of Penfield that's well worth reading, by the way.

As I said in my answer to:

Are all the wrinkles on a brain's cortex the same across people?

...neurosurgeons will perform electrical stimulation mapping of awake people if they have to remove any brain tissue near what they call "eloquent cortex"... [because] [t]he only way even an experienced surgeon can be sure that specific brain area in a specific person is motor, or speech, or sensory, is via this mapping technique... This is because, although gross neuroanatomical features are generally conserved across people, there can be a huge range of variation.

Penfield used a highly invasive means to map out the motor homunculus. But it turns out we have some pretty cool modern technology with which we study the motor cortex non-invasively: Transcranial Magnetic Stimulation (TMS).

TMS induces an electrical current using a rapidly changing magnetic field.

Pictures speak volumes:

As do videos. Watch the TMS disrupt conscious motor control:

The stimulation of the motor cortex by the TMS sends a "fake" signal to the hands, causing muscular contractions. (MEP is "motor evoked potential": the electrical signal recorded from the hand muscles.)

By combining TMS with individual MRIs, we can get relatively fine mapping between TMS and the brain.

In 1995 a group of neuroscientists published a paper called, "Modulation of muscle responses evoked by transcranial magnetic stimulation during the acquisition of new fine motor skills" in the Journal of Neurophysiology.

In this paper, they showed that they could map the amount of motor cortical territory devoted to specific fingers.

The authors had their subjects train on a piano and mapped motor cortex finger representation before and after training. Here's what they found:

Over the course of 5 days, as subjects learned the one-handed, five-finger exercise through daily 2-h manual practice sessions, the cortical motor areas targeting the long finger flexor and extensor muscles enlarged, and their activation threshold decreased.

Thus, they demonstrated that even adults show cortical plasticity after some simple muscle training. That is, piano practice caused the amount of brain devoted to voluntary muscular control grow.

So although you may not currently be able to flex your ring finger or control your individual toes, there's no reason that you can't learn how!

Amputees, for example, can learn to be quite dexterous with their toes.

Here's a man writing perfectly well:

And a woman demonstrating how she bathes:

So to (finally!) answer your question: you can't control your toes because you haven't practiced, and therefore the "toe" area of your motor cortex is too small to allow fine control.

Exercise your brain's plasticity and practice writing with your toes! Get back to me after a few weeks of practice and let me know how it went.

For science!

(Note, some of the above images probably came from my friend and zombie collaborator Timothy Verstynen many moons ago during our PhDs.)

Pascual-Leone A, Nguyet D, Cohen LG, Brasil-Neto JP, Cammarota A, & Hallett M (1995). Modulation of muscle responses evoked by transcranial magnetic stimulation during the acquisition of new fine motor skills. Journal of Neurophysiology, 74 (3), 1037-45 PMID: 7500130
Penfield, W., & Boldrey, E. (1937). Somatic motor and sensory representation in the cerebral cortex of man as studied by electrical stimulation Brain, 60 (4), 389-443 DOI: 10.1093/brain/60.4.389

Zombies (and me!) at the California Academy of Sciences NightLife!

2011-09-27T11:09:00.000-07:00

You like zombies? Of course you do.
You like science? Who doesn't?!!

Well this October 27 the California Academy of Sciences will have yours truly giving a talk at their ever-so-popular NightLife event!

I'll be bringing real human brains for a hands-on neuroanatomy demonstration!

I'll also be talking about the zombie brain and how neuroscience can help you and your loved ones survive the zombie apocalypse! :D

Seriously this is going to be a lot of fun: there will be a zombie drag show and costume contest, undead makeup artists, demos of the new zombie video game hotness Dead Island, and a special planetarium event about "zombie" stars.

Buy tickets now!

Thinking with Portals

2011-09-26T08:58:00.000-07:00

My love for Portal, Portal 2, and video games in general is certainly no secret. Nor is my love for comics and other geekery.

Recently I played through the Portal 2 single- and multi-player campaigns (with my Activision and Call of Duty buddy, Bryan).

I love the Portals.

(Screenshot from Portal 2)

Of course, me being... well... me, I couldn't help but think about why I loved the game and then a bunch of weird brainy neuro stuff.

Basically the end result of my over-intellectualization was that sometimes games are just fun.

That's it. End of post! Hope you enjoyed it.

.
.
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Oh. You're still here? ::sigh::

Okay,I guess I can continue on. For science. Or rather, for neuroscience.

If you're unfamiliar with the Portal games, a wonderfully homicidal AI is trying to murder you in the name of advancing science. Your goal is to stay alive by surviving her tests using only a gun. But this is a special gun. It creates portals that allow you to teleport between portal A and portal B. Momentum, a function of mass and velocity, is conserved between portals. In layman's terms: speedy thing goes in, speedy thing comes out.

This game has some ridiculously crazy 3D spatial reasoning puzzles and I got to thinking about how the hell I was able to shoot a portal at a wall, shoot another across the room, and know that when I went into one I would come out the other. There's a lot going on here to let the brain do this!

Seriously, some of these puzzles are mind-bending. Watch this speed run:

Get all that? There's a reason why scicurious gets motion sick when she tries to play the Portal games.

(As an aside, it also contains one of the best end game songs ever, written by Jonathan Coulton.)

In this post I'll give a brief introduction about how the human brain can even conceive of teleporting between two portals. More specifically I'll talk about visual attention and working memory. You can't really conceive of moving from portal A to portal B without first knowing where the two portals are relative to each other and to the room you're in.

I want to make it clear how hard it is to study something like spatial attention and memory. These concepts are more metaphors or placeholder terms we use in neuroscience to describe observable psychological and behavioral phenomena than actual brain processes. They're kind of ill-defined and nebulous, though there's a massive literature that attempts to unite the behavioral with the neuronal.

The first mind-blowing spatial attention thing to know about is hemispatial neglect. The most common form of hemispatial neglect results from damage to the right posterior parietal lobe. It manifests as the inability to conceive of or see one visual hemifield.

What does that mean?

Well, check this out:

Literally, there is no conception of "leftness".

The above examples are of two drawings from a patient with hemineglect. Notice that, when copying a drawing, the patient is missing the whole left half of the object. And when free drawing, they show a similar effect. There's a great review on this topic by Masud Husain and Chris Rorden from 2003 in Nature Reviews Neuroscience.

In that paper the authors do an amazing job summarizing what we knew about neglect at the time. I'll also take this moment to emphasize yet again how much we've learned about human cognition from work done with patients with brain lesions.

Visual attention is an enormously huge domain that strongly overlaps with research into visual working memory.

The thing about working memory is that there's a lot of controversy in the field about well, how it works. There's a really cool researcher by the name of Paul Bays (who worked with Husain of the previously-mentioned paper) that summed up the debate very succinctly in the introduction of a 2009 paper they wrote in the Journal of Vision:

The mechanisms underlying visual working memory have recently become controversial. One account proposes a small number of memory "slots", each capable of storing a single visual object with fixed precision. A contrary view holds that working memory is a shared resource, with no upper limit on the number of items stored; instead, the more items that are held in memory, the less precisely each can be recalled.

This all stems from George Miller's famous paper from 1956, The magical number seven, plus or minus two: some limits on our capacity for processing information (decent Wikipedia summary here).

Anyway, visual attention and working memory are extremely difficult to disentangle. You can see the strong relationship between the two concepts in brainSCANr:

(In fact, I believe a big chuck of working memory research is conflated with attention... I've got a project to try and demonstrate just that).

The number of experimental paradigms used to study attention and/or working memory is enormous so, although there are fairly "standard" paradigms, even slight differences between stimulus presentation, timing, task, etc. can lead to fairly big differences in results.

However, the visual experiments that require a person to sit in a darkened room while some images flash at them on a computer screen has lead a number of researchers to call into question what is actually being tested in these situations. Does remembering when an X appears on a screen really encapsulate human memory? Does noticing a green square in a sea of red squares typify attention?

Of course, more ethological ("real-world" scenario) experiments sacrifice control for validity... making the whole damned thing a mess.

But this messiness is part of the allure... if it was easier we'd have figured it out decades ago and I'd be out of a job! :)

Husain, M., & Rorden, C. (2003). Non-spatially lateralized mechanisms in hemispatial neglect Nature Reviews Neuroscience, 4 (1), 26-36 DOI: 10.1038/nrn1005
Bays, P., Catalao, R., & Husain, M. (2009). The precision of visual working memory is set by allocation of a shared resource Journal of Vision, 9 (10), 7-7 DOI: 10.1167/9.10.7
Miller GA (1956). The magical number seven plus or minus two: some limits on our capacity for processing information. Psychological review, 63 (2), 81-97 PMID: 13310704

"Peer-review" does not equal "publisher-owned journal"

2011-09-22T09:12:00.000-07:00

Yesterday was my first real day working at UCSF. Most of it was spent filling out paperwork and completing all of the regulatory training.

For those of you unfamiliar with the regulations required for human research, let me just say that they are legion, for they are many. In order to work with human subjects you have to (among other requirements) complete several online courses and questionnaires.

This is usually all well and good if not a bit annoying... (Yes, I know I shouldn't inject my subjects with radioactive spider venom without their consent. No, I didn't consider that radioactive spider venom would be an Investigational New Drug. Yes, I disclosed my consultancy income from OSCORP.)

Anyway, many universities such as UCSF, Berkeley, etc. require researchers who work with human subjects to complete their online training on a specific website: the Collaborative Institutional Training Initiative.

For example I had to complete the "CITI Good Clinical Practice", "Human Subjects Research", and the "Responsible Conduct of Research" curricula. While answering questions in the latter, I encountered the following (which I got "wrong"):

(Someone needs to "peer-review" the inconsistant capitalization in the headers and that superfluous comma in that "Comment".)

This question struck me as especially odd. "Why," I asked, "is this unscientific, unsubstantiated question here? Are they afraid that researchers will stop publishing their research in peer-review and just BLOG everything?"

Does "those who have an interest in the work" not include peers? Have the authors not heard of arXiv.org?

Of course "BLOGS" aren't a replacement for peer-review. Blogs can be peer-reviewed, though, and "peer-review" is not equivalent to a publisher-owned journal. Where does the line between "blog" end and an online journal with commenting begin?

As Bora said over at the SciAm blogs:

Blog is software. Blog is primarily a platform. It is a piece of software that makes publishing cheap, fast and easy. What one does with that platform is up to each individual person or organization.

He points out the open science approach by Rosie Redfield as an example of peer-review that can be moved onto a blog to some extent.

Blogs may not replace peer-review, but they are certainly part of it already.

As was pointed out in a Nature News piece:

To many researchers, such rapid response is all to the good, because it weeds out sloppy work faster. "When some of these things sit around in the scientific literature for a long time, they can do damage: they can influence what people work on, they can influence whole fields," says [David] Goldstein.

Personally, I use my blog for many things. I talk about my own research a lot.

But I also post some fun, off-the-cuff ideas and analyses that, were I more motivated and had infinite time, I could probably polish and write up for peer-review.

It doesn't make those ideas less valuable, just more rough. And I hope someone takes some of them and runs with them. But of course, a major issue here is one of idea attribution.

As Ben Goldacre said in his Correspondence to Nature:

The growth of blogs, Twitter and free online access have caused a welcome explosion in scientific content. But this is atomized and interconnected by a hotchpotch of linking and referencing conventions. If we are going to harness its true value, we shall need dedicated librarians and information scientists to find ways of automating the process of linking content together again. That in itself would be a transgressive scientific innovation.

The current academic reward structures don't give me anything for this blog. So in the meantime I'll continue doing research with people and publishing it in "real" peer review while rolling my eyes at the occasional awkwardness with which academia approaches technology.

Goldacre, B. (2011). Harnessing value of dispersed critiques Nature, 470 (7333), 175-175 DOI: 10.1038/470175b
Mandavilli, A. (2011). Peer review: Trial by Twitter Nature, 469 (7330), 286-287 DOI: 10.1038/469286a

Thank you Mario! But your methods are in another field!

2011-09-16T14:48:00.000-07:00

My love for video games is no secret. I just finished Mass Effect 2 and started Dragon Age 2 (I'm a sucker for Bioware RGPs).

One of the first true peer-review papers I remember reading was Green & Bavelier's 2003 Nature paper "Action video game modifies visual selective attention". In that study the authors performed a series of experiments showing that people who had a lot of experience playing "action video games" performed better than non-video game players on a variety of attention tasks. Particularly striking, for example, was just how much better gamers did on a spatial attention task. Check it out:

I mean, look at that! Not even close (VGP = video game players; NVGP = non-VGP). Gamers blow non-gamers out of the water.

So my interest was especially piqued by some news going around today published on Nature's site (written by Mo Costandi) stating that "Video-game studies have serious flaws: Poor design of experiments undermines idea that action games bring cognitive benefit".

Oh. Snap.

Them's fighin' words!

Mo's article references a new Perspective just published in Frontiers in Psychology by Boot, Blakely, and Simons (open access!)

In it the authors note that cognitive transfer studies are quite contentious (see, for example, last year's Owen et al. Nature paper "Putting brain training to the test").

So what are the issues with the video game studies, according to Boot, Blakely, and Simons? They ennumerate 5 separate issues:

Overtrecruiting (possible differential demand characteristics)
Unspecified recruiting method
Potential third-variable/directionality problems (cross-sectional design)
No test of perceived similarity of tasks and gaming experience
Possible differential placebo effects

So basically they're saying that these video game studies aren't using the proper research methodology.

They note that:

Claims that gaming causes cognitive improvements require an experimental design akin to a clinical trial; in this case, a training experiment.

It amazes me how many meta peer-review papers are written that simply reiterate basic research and/or statistical methodologies.

Another recent example of this was a paper in Nature Neuroscience (!) last week by Nieuwenhuis, Forstmann, and Wagenmakers ("Erroneous analyses of interactions in neuroscience: a problem of significance") whose entire point basically boils down to: use an ANOVA to test for interactions.

This is stats 101! Hell, it's stats 001! (Ben Goldacre did a great piece on this in the Guardian).

I don't get why these things have to be re-explained every few years. These things just reinforce how domain-specific many academics are in their knowledge (and why I think branching out is so important).

In 2006 there was a paper in The American Statistician by Gelman & Stern titled "The Difference Between “Significant” and “Not Significant” is not Itself Statistically Significant".

Same basic stats issue as the one that Nieuwenhuis, Forstmann, and Wagenmakers got into Nature Neuroscience just 5 years later.

I mean I write papers wherein I get locked in detailed, intricate statistics battles with reviewers. Apparently the trick is to just fail at the most low level possible?

But seriously I'm not calling any of the video game studies bad; nor do I think were Boot, Blakely, and Simons.

Science is iterative and it's important to publish, even if the methods and data aren't perfect.

Embrace the imperfections and failures!

That's how this science stuff works.

But it would be nice if the failures weren't so, uh... basic?

Green CS, & Bavelier D (2003). Action video game modifies visual selective attention. Nature, 423 (6939), 534-7 PMID: 12774121
Boot, W., Blakely, D., & Simons, D. (2011). Do Action Video Games Improve Perception and Cognition? Frontiers in Psychology, 2 DOI: 10.3389/fpsyg.2011.00226
Owen, A., Hampshire, A., Grahn, J., Stenton, R., Dajani, S., Burns, A., Howard, R., & Ballard, C. (2010). Putting brain training to the test Nature, 465 (7299), 775-778 DOI: 10.1038/nature09042
Nieuwenhuis, S., Forstmann, B., & Wagenmakers, E. (2011). Erroneous analyses of interactions in neuroscience: a problem of significance Nature Neuroscience, 14 (9), 1105-1107 DOI: 10.1038/nn.2886
Gelman, A., & Stern, H. (2006). The Difference Between “Significant” and “Not Significant” is not Itself Statistically Significant The American Statistician, 60 (4), 328-331 DOI: 10.1198/000313006X152649

Uberdata: How prostitution and alcohol make Uber better

2011-09-13T11:19:00.000-07:00

As some of you know, I've been doing some work for a transportation startup in San Francisco called Uber (prior to starting my post-doc at UCSF).

Weird job for a neuroscientist, I know. But I'll explain why in a bit.

I don't want this post to sound like an advertisement for them, but I think a lot of the readers of this blog (who are here for the neuroscience) might find my most recent blog post for Uber interesting. And you might also find why I'm working with them interesting.

Academia ia great. I love it. But there's a certain lethargy and insularity that I wanted to break out of for a bit. Working at an awesome, tech-driven startup with kick-ass engineers for 3 months was an amazing experience. My startup sabbatical. And I learned a lot of data storage, retrieval, and analysis techniques--as well as gaining some new programming skills--that I just wouldn't have gotten out of academia.

Part of what I've been doing for Uber is writing data-driven blog posts. I think the most recent one is pretty wild. So here's the post in its entirety, but you can read it over on the Uber blog here.

*****

What up humans?! Bradley Voytek here again. Man do we have some crazy #uberdata for you today.

Today is Uber: Freakonomics edition.

In this post I'll show how where crimes occur—specifically prostitution, alcohol, theft, and burglary—improves Uber's demand prediction models.

As you know, the three of us in Uber team Science (below) are pretty busy nerding it up around the Uber offices all day adding numbers together, pouring colored liquids into beakers, that sort of thing.

One of the most important jobs we do (second only to keeping our Uber Science mutants securely locked up) is to accurately predict demand to make sure you get a car when you want one. We've managed to do this pretty well so far, but we're continually making tweaks to improve things.

One way of predicting demand is by knowing when people want to ride with us.

Another factor is knowing where people will want rides. Our drivers have a pretty intuitive understanding of this, but we believe that math makes everything better, so we wanted to have some quantification.

This is a harder problem.

But a few weeks ago I attended Sci Foo at Google and got a ton of crazy, dirty #dataporn ideas.

As you know, location is important to us because proper supply positioning lets us reduce pickup times. For example, we're obviously going to see an increase in trips in SoMA near AT&T Park before and after Giants games.

The first issue we encountered is determining an easy, intuitive way to break a city into discrete "places". While mathematically this isn't necessary, in terms of communicating the data internally it's very important.

Thanks to Zillow we were able to extract the complex boundaries for neighborhoods in each Uber city. Check out the 34 neighborhoods in San Francisco:

First: shut up. I don't care if your neighborhood isn't part of that map. I know that the Tender Nob is sick. But if I had to figure out all of the boundaries of all of the sub-sub-sub-neighborhoods of San Francisco, I'd be able to figure out the length of the British coastline (nerd joke).

Unfortunately figuring out whether or not a geographic point is inside one of those complicated shapes is complicated.

Haha, just kidding. We got this.

The first thing we did was to look at how many trips we've done per neighborhood. Check it out:

(Map colors based on www.ColorBrewer.org, by Cynthia A. Brewer, Penn State.)

Uber Mondrian!

Here's Manhattan (and Williamsburg):

You'll notice that we do the most San Francisco trips in the downtown and SoMa areas. These also happen to be large, densely populated regions, so that's to be expected. So in our spatial demand predictions we clearly need to take into account population density.

But there's a catch. While neighborhood population density might account for some of the variance in our demand, we also need to take into account where people are hanging out, going to work, etc. This is different from census data. Where people live, where people work, and where people play are (usually) in very different neighborhoods in a densely populated city.

So we needed a simple surrogate metric for where people are. We could do that by counting the number of businesses or bars or whatever in a neighborhood... but we had a better idea.

Crime.

We hypothesized that crime would be a proxy for non-residential population density.

According to the data from San Francisco Crimespotting (HUGE shout-out to Stamen Design for the data; you guys are awesome!), there were 75,488 crimes in San Francisco since Uber's launch on 2010 June 01. These crime data are broken down into 12 categories: murder, robbery, aggravated assault, simple assault, arson, theft, vehicle theft, burglary, vandalism, narcotics, alcohol, and prostitution.

Let's map that:

If it looks kind of like the trips map to you, that's because the two are decently correlated (r = 0.56, p < 0.001). (For you math sticklers, crime and trip data are log distributed by neighborhood, so all correlations are Spearman rank correlations, but log-log Pearson correlations give approximately the same results).

Neighborhoods with more crime (more people hanging out) have more Uber rides.

But we also wanted to know if any specific crimes might be better predictors of rides than others.

To examine this we looked at the correlation between the number of each type of crime and the number of trips we've done in each neighborhood. All types of crime except murder, vehicle theft, and arson were positively correlated with number of trips. After correcting for multiple comparisons, four crimes remained significantly correlated (p < 0.05, Bonferroni corrected):

Prostitution
Alcohol
Theft
Burglary

In other words:
The parts of San Francisco that have the most prostitution, alcohol, theft, and burglary also have the most Uber rides! Party hard but be safe, Uberites!

Of course this isn't in any way causal. I don't think our Uber riders are causing more prostitution. Right guys?

Like I said above, this effect probably reflects population density in terms of where people socialize: the more people that are hanging out in an area, the more prostitution, alcohol, and theft there is. Makes sense.

Now, let's go back to the timing thing. We know that Uber rides change by hour and day of week. What about crime?

Across all crimes there's not much variation in the total number of crimes between days. However within a day there's a lot of ups and downs. It turns out that the number of crimes peaks between 6 and 8pm.

But there was one surprise. One crime, beyond all the rest, had a specifically BIG peak on a specific day.

Prostitution.

On Wednesday nights.

This was so surprising to me that I doubled-checked the effect by looking at crimes in Oakland, too. Oakland Crimespotting also had a lot more data: 152,730 crimes in the database since 2008 Jan 01.

We got the same effect. Check out Oakland's data:

Now mind you, at this point I've strayed from the Uber ride-prediction path. Crime is a good proxy for the "activity" of a city, but the timing of the crimes doesn't really correlate with our ride patterns.

From here on out in this post, everything is purely for my love of #dataporn and my inner scientist getting all giddy with a neat effect. This was just too fascinating of a finding for me to let go (I'm a scientist, dammit!) I needed to figure out why.

Why Wednesday nights?!

Hell, I even stopped to talk to two cops in Berkeley to see if they knew of any reason why prostitution crimes peaked at this time (seriously). They had no idea. And they probably thought that the weird math nerd babbling to them about statistics and prostitution was off his nut.

But then someone pointed out to me that Social Security and welfare checks arrive on the second, third, and fourth Wednesdays of each month.

Oh man. Now I've gotten myself into dangerous, politically-charged territory.

Keep in mind we're only talking about 4-5 prostitution crimes each Wednesday. This is pretty low considering the cities we're talking about have populations in the hundreds of thousands to millions. So before you go running off screaming about how the welfare state is subsidizing sexy times for retirees, chill out and keep that in mind.

It turns out that there are significantly more prostitution crimes on the second Wednesday of each month compared to the first (p < 0.01):

Why? Well one possibility is that on the second Wednesday, people get their checks after two weeks without any income. The first Wednesday: no checks. Second Wednesday: cash in hand!

It might be that any time there's an influx of cash into a city, there's also a bump in prostitution crimes. That's harder to check, but worth following up.

Mind you, I don't see this effect for any other types of crimes. Just prostitution.

This doesn't prove anything conclusively, of course. And again, we're talking about a difference of, on average, only a few extra cases of prostitution. But because we have so much data we can get a good assessment of the statistical significance of this effect.

This one of the coolest things about working for a data-driven company like Uber: on the surface we're a transportation company, but below the hood there are so many ways to look at our data. And sometimes that freedom to play leads to interesting results.

This finding is a perfect example of the fascinating insights you can get when you combine big datasets. By trying to figure out how to predict where to position our cars, we got a peek at the ebb and flow of the life and crimes of San Francisco. Expect more of these kinds of posts in the next couple of weeks.

We've got a lot of cool stuff in store, I promise you!

A case of sexually-transmitted, self-organized neurogenesis

2011-09-08T16:39:00.000-07:00

4kg and 51cm

:D

Can brain trauma cause cognitive enhancement?

2011-09-05T10:12:00.000-07:00

Another post inspired by Quora. Someone asked the question: "Can brain trauma cause cognitive enhancement?".

Obviously this topic is dear to me, so I felt compelled to answer.

(Read previously on my TEDx talk, my Neuron paper on functional recovery after stroke, my PNAS paper on working memory network deficits after stroke, why we don't need a brain, and my discussion of Rep. Grabrielle Giffords' brain surgery).

The full response to the Quora question is below.

*****

Maybe! But most likely only in very specific cases of brain damage, and only for very specific types of cognitive task.

In 2005, Carlo Reverberi and colleagues published a really cool peer-reviewed paper in the journal Brain:

Better without (lateral) frontal cortex? Insight problems solved by frontal patients. Reverberi C, Toraldo A, D'Agostini S, Skrap M. Brain. 2005 Dec; 128(Pt 12):2882-90.

They studied patients with damage (lesions) to the prefrontal cortex:

They had these patients perform an "insight"-based task. Very simply subjects were given a math problem arranged in toothpicks. The goal was to make the arithmetic work by only moving one toothpick.

Visually:

So for the very first problem, you can see it starts by saying "4 = 3 - 1" which is clearly wrong. But by moving one of the toothpicks in the equal sign over to the minus sign, you swap the two, making an arithmetically sound equation: "4 - 3 = 1".

Without getting into a ton of details, it turns out that in some very specific cases, patients specifically with lateral prefrontal damage performed better than people without brain damage.

The theory behind this sort of fits with what we know about decision making and expectation. Basically, because of these patients' lesions they have some deficits in using contextual information and internal cues to inform their decision-making. But in a difficult task such as this with a large "search space", rather than getting stuck in specific patterns, they're a bit more "freed up" from internal expectancies and thus can hit on the correct solution more quickly.

Reverberi, C. (2005). Better without (lateral) frontal cortex? Insight problems solved by frontal patients Brain, 128 (12), 2882-2890 DOI: 10.1093/brain/awh577

Career... advice?

2011-08-16T09:38:00.000-07:00

Back in June, someone over on Quora specifically asked a question of me: "What advice would Bradley Voytek give to undergraduates on studying and researching neuroscience?"

It took me a while to respond for several reasons, not the least of which is that I'm super busy. And also because it felt kind of weird to answer. I mean, I didn't study neuroscience as an undergrad. And I didn't do well as an undergrad. So I certainly shouldn't be doling out advice!

But the beauty of hindsight is that its glasses are often rose-tinted. So I sat down an answered as best I could while trying to avoid platitudes and cliches. My full response is below.

This is a really tough question, because it's so broad. I'm not really sure how to answer it. Because I'm more of a cognitive/systems/computational neuroscientist, I'll approach my answer from that direction.

My wife and I were talking about this recently after watching Freakonomics. She was asking me what classes I was good at in high school. I was a great high school student without really trying to be, but I quickly became a bad college student, mostly because I started learning how to socialize.

What happened to me, I think, was that once I started doing poorly in college while my friends continued to succeed, I started to think I wasn't cut out for college. I started to think I was a hack.

Only much later would I learn of something called "impostor syndrome".

Anecdotally, this appears to be fairly rampant among academics and other "smart" people. At some point during your career, possibly more than once, you will look at your peers and think to yourself, "I'm not as good as they are; I am not cut out for this."

So my first few pieces of advice will be academically related, but not neuroscience specific.

First: listen to that voice. Understand where it's coming from. But be aware that you're failing to recognize your own accomplishments; you're overemphasizing the accomplishments of others and you're vastly underestimating the failures other successful people experience on their way to success.

It's for that last reason that I've been including an entire section in my CV (PDF) called "Failures and Rejections" that includes rejected grant applications, rejected publications, rejected grad school applications, etc.

It's important to me that other people know how hard this life, science, and career stuff really is. People should know that often, success doesn't come easy.

The second piece of non-specific advice: learn to network. Talk to other researchers. Email people about their work when you have questions. Don't be shy. Or rather, go ahead and be shy but recognize that lots of people are shy and the only way to learn from them is to overcome your mutual shyness. Plus, researchers love to know that someone read their work and are interested.

This advice isn't meant as a machiavellian ploy or anything. Networking lets you meet smart people, which gives you new ideas and new collaborations. This, in turn, lets you do science faster and better.

Networking is sharing, not manipulating.

Third: learn how to do your own data analysis. Know statistics well. Know at least some basic programming/scripting in Python, R, Matlab, etc. This will be of immense value in helping you get your research done efficiently and correctly, without needing to rely on other people's code (and time and commitment). This will become more important as our field becomes more data driven.

Ok, now the neuroscience specific advice.

Most importantly, I'd have to say not to buy into the false belief that many neuroscientists seem to carry that somehow we actually know what the brain is doing.

Understand that most neuroscientific "facts" are inherently making statistical, not factual, statements. Broca's area is probably involved in language production, insomuch as there is a brain region that can be clearly identified as "Broca's area" in any one given person. There's a reason why neurosurgeons do electrical stimulation mapping prior to tissue resection. (See Are all the wrinkles on a brain's cortex the same across people?)

Think critically about any statements you encounter in the neuroscientific literature and in your own thinking; e.g.:
What does it *mean* for a brain region to be "involved in a task"?

Can you have neural correlates of a behavior without needing that neural region?

How are the researchers operationalizing "attention", "memory", "emotion", etc.? Are they measuring what they say they're measuring?

What does a neuron do? Seriously. Think about this one hard.

Look to the literature *before* you start your research. A lot of cool single-unit work was done in the 1960s and 70s that's been forgotten.

But don't mistake old research as Truth, either.

I could do this all day, but hopefully this will give you a feel for what I think is important in terms of how I approach my research.

I've written a few pieces of neuroscience skepticism before as well, if you want to delve deeper. For example: "How to be a neuroscientist".

Feel free to email me if you want to know anything more specific. I'm always happy to chat.

Final piece of advice:

Everything I've said is anecdotal experience about my own life and my own path, and thus should be treated with as much skepticism as anything else.

CDC, zombies, and Comic-Con

2011-08-11T14:51:00.000-07:00

Just a quick update this afternoon.

First, if you haven't seen the new zombie work by the CDC, check it out! It's from the Office of Public Health Preparedness and Response. Posters were available for free, but they appear to be out of stock now...

You can still download very high-res versions, however.

Next, my interview video with Wired from Comic-Con has been posted online! I have to say I was pretty uncomfortable. I was extremely busy and stressed from work at the time, and took a quick trip downstairs from my hotel room to check out the Wired party that my friend (and Wired writer) Angela invited me to.

Five minutes later I was in a tent off from the main pool party area getting interviewed. I'm just wearing a dirty white t-shirt, and I'm clearly not in my element.

The article's nice though, so I can't complain!

Self-stimulating the brain for heterosexual sex with a prostitute. Seriously.

2011-08-07T20:09:00.000-07:00

Deep brain stimulation is such a cool, successful, amazing piece of technology, that I was excited to read a little more about its historical roots. But man. I don't even know what to say now.

I've written about a lot of crazy neuroscience stuff on this blog over the last 20 months:

But this... is the weirdest, most shocking research I've read, bar none. Literally, the litany of crazy shit in this paper is so long that by the end my reading, my notes in the margin devolved to this:

A while back, someone pointed me to a paper from 1972 by Dr. Robert G. Heath titled "Pleasure and brain activity in man: Deep and surface electroencephalograms during orgasm".

"How fun," I thought to myself, so very, very naively. "This will be a nice complement to my post about EEG and orgasms." (I'm quite proud to say these are the flavor of thoughts that I have.)

Instead, I got this unethical marvel.

The first thing I noticed was that 15 out of the 18 works cited in this manuscript are self-citations. That is, 83% of the previous research that this paper was built upon was written by the author himself.

"That's odd," I mused, "probably not the best sign."

To give a little background, this paper was written by Robert G. Heath. I didn't really know anything about this guy, but he was notable enough to have received an obituary in the New York Times. According to that (short) article:

In 1957, Dr. Heath found a protein antibody called taraxein in the blood of schizophrenics that was capable of inducing schizophrenic-like symptoms in monkeys and healthy human volunteers.

The finding was controversial because it was early evidence that schizophrenia is of biochemical origin and not, as was widely believed at the time, related to childhood or other emotional traumas.

Ok, fine. That's nice. But what's weird--and what the New York Times obit doesn't say--is that the taraxein theory of "schizogenesis" appears to be total crap, despite the fact that Heath held fast to his claims. Furthermore, the ethics of this research are questionable, at best. As Professor Alan Baumeister wrote in his historical analysis "The Search for an Endogenous Schizogen: The Strange Case of Taraxein":

On May 3, 1956... Heath announced that he and colleagues "had induced full symptoms of schizophrenia" in two nonpsychotic prisoner-volunteers... by injecting them with an extract from blood of schizophrenic patients.

(All emphases in this post's quotations are mine.)

If you've ever done research, or have any sense of ethics, the thought of using prisoners in an experiment to see if you can induce psychosis should set off your humanity-alarms.

What's more, according to Wikipedia (the arbiter of all Truth, I know):

Heath founded the Department of Psychiatry and Neurology at Tulane University, New Orleans, in 1949 and remained its Chairman until 1980. He performed many experiments there... [and] was partially financed by the CIA and the US military. One of his collaborators... later reminisced that they had used African Americans as subjects "because they were everywhere and cheap experimental animals".

You stay classy, history of psychiatry.

You'll note that all these things I've talked about so far? Nothing to do with the paper I intend to discuss. All this stuff? This is just flavor text to set the stage for the really unethical stuff.

Needless to say, Heath and his research will likely be the topic of several posts here.

So, back to orgasms and prostitutes. I'm not even going to bother trying to explain the scientific aspects of this paper. The hypothesis, methods, results... none of it matter because they're just completely overshadowed by every crazy part about this research.

I'm just going to quote huge swaths of this paper and let you all say, "WHAT THE HELL!!?"

In patient B-19, a man, EEG's were obtained on two occasions when this arousal culminated in orgasm: once, as a consequence of masturbation and once through heterosexual intercourse.

Okay, that's kind of weird on its own, but hey, the research could be very interesting. I mean, the patient had electrodes implanted under his skull. This is usually done to determine where exactly in the brain the source of seizure activity is. This method is still used, and working with these patients is a major component of my research.

And sex research is fascinating! So if you've got someone in this situation, and they agree without any kind of coercion, then why not?

Wait, what's that Dr. Heath? This patient is homosexual? Oh...

Well please, tell us more about the patient and your experiments.

This man... had a 5-year history of overt homosexuality and a 3-year history of drug abuse. He was considered a chronic suicidal risk... and had made several abortive suicidal attempts... One month of military service... was terminated by medical discharge because of "homosexual tendencies"... The patient's experimentation with drugs began... with ingestion of vanilla extract. He became habituated to amphetamines, and he had used a variety of other sedative and hallucinogenic chemicals (marijuana regularly, nutmeg frequently, d-LSD sporadically, as well as inhalants, such as glues, paints, and thinners, and sedatives).

This is to set the stage. This patient has severe epilepsy, is a drug addict, and is extremely depressed.

So what does Heath do next?

...the patient was equipped with a three-button self-stimulating transistorized device... The three buttons... were attached to electrodes in the various deep [brain] sites, and the patient was free to stimulate any of these three sites as he chose... He was permitted to wear the device for 3 hours at a time: on one occasion he stimulated his septal region 1,200 times, on another occasion 1,500 times, and on a third occasion 900 times. He protested each time the unit was taken from him, pleading to self-stimulate just a few more times... the patient reported feelings of pleasure, alertness, and warmth (goodwill); he had feelings of sexual arousal and described a compulsion to masturbate.

For those of you who don't know, this type of behavior was seen in rats in the original brain stimulation and reward experiments by Olds and Milner. Rats self-stimulated sometimes to the point of death.

Seems like a perfect situation for a heavy drug addict, right? Just let him stimulate the "reward" and "pleasure" parts of his brain for hours on end!

But wait! There's more!

One aspect of the total treatment program for this patient was to explore the possibility of altering his sexual orientation through electrical stimulation of pleasure sites of the brain. As indicated in the history, his interests, contacts, and fantasies were exclusively homosexual; heterosexual activities were repugnant to him.

He's gay. Very clearly gay. And his brain is getting forcibly stimulated such that he's experience strong sensations of sexual pleasure.

A twenty-one-year-old female prostitute agreed, after being told the circumstances, to spend time with the patient in a specially prepared laboratory.

A "specially prepared laboratory"? Nice. Did the doc light some candles?

And where did they get the prostitute? How did that conversation go?

Scene: 1970s, late night; car rolls up to young woman standing under a streetlight; window rolls down as car approaches

"Excuse me, miss? My name is Dr. Heath. I've got a young, gay man hooked up to a brain stimulator back in the hospital. He's been stimulating himself stupid horny these last few days. If I give you $40 would you mind coming back with me and see if you can't screw him straight-wise? Be sure to mind the wires because they're hooked right into his brain.

Can you imagine writing this into your IRB proposal? I mean. What?

And I love the matter-of-factness about describing how this all played out:

The laboratory was modified to permit complete privacy, and an extension cord was inserted between the plugs in the patient's hand and the jack box to the recording room to give him adequate mobility.

He goes on:

Later, the patient began active participation and achieved successful penetration, which culminated in a highly satisfactory orgiastic response, despite the milieu and the encumbrances of the lead wires to the electrodes.

To recap: this study involved taking a severely depressed, drug addicted, gay man into the hospital, letting him stimulate his own brain, and then tracking down a prostitute to have sex with him.

This is the most boggling, unethical, and offensive piece of "research" I've ever come across. I can't imagine what the rest of the papers by this guy are like.

If anyone has seen anything in the peer-review literature that's worse, I'd like to hear about it.

Heath RG (1972). Pleasure and brain activity in man. Deep and surface electroencephalograms during orgasm. The Journal of Nervous and Mental Disease, 154 (1), 3-18 PMID: 5007439
Baumeister A (2011). The search for an endogenous schizogen: the strange case of taraxein. Journal of the History of the Neurosciences, 20 (2), 106-22 PMID: 21480035

The role of Facebook and Twitter in scientific citations and impact factors

2011-07-21T08:14:00.000-07:00

This past weekend I was messing around on the internets (when I should have been relaxing by a river) when I was struck by a question: is there a way to see what impact social media has had on science?

Turns out, social media such as Facebook and Twitter may have a big influence on journal impact factors and paper citations... but more on that in a second. (For a primer on impact factor and citations, read my old post: "Something ghoti with science citations".)

First: my rambling thoughts.

Many of us scientists have this perception that "social media" is "important" for science, but I don't yet have a grasp on what that means, and I don't think anyone else does, either.

In fact, just yesterday over on Wired, @Sheril_ asked a bunch of science twitterers why they use Twitter. The responses are all over the place! People use it for self promotion, for sharing and learning new ideas, for staying in touch, professional networking, etc.

I've talked about the role of various social networking/Web2.0 sites in the scientific process ad nauseam. I've espoused my interest in Quora in my post "Quora for Scientists":

...with Quora, anyone can connect with potential experts. The question is how can Quora engage these experts? Why would anyone contribute their expert knowledge for free? I mean, I do it because... well I really enjoy talking with the public about science. Sometimes it's the really simple questions (e.g., What is the neurological basis of curiosity?) that really make me stop and think about "easy" questions I normally wouldn't worry about. That's exciting to me. I like to solve hard problems (especially ones that seem easy), and I think most scientists feel the same way.

Again, that's just another opinion. Another rationale added to many others.

But what do the data suggest?

I turned to the ISI Web of Knowledge, which provides excellent journal-specific metrics such as the total number of citations a journal has received, the journal's impact factor, and so on. (Sadly these metrics are closed to the general public; you need a license to view them.)

For each journal I got its 2010 impact factor as well as the total number of citations the journal has received. The former measures the average number of times a paper published in that journal was cited between 2008 and 2010. The latter is more of a "popularity" measure weighted by the number of publications in the journal.

I wanted to see what impact social media has on these two common metrics. To do that I looked to Facebook and Twitter to find which journals have their own Facebook pages and Twitter accounts. In the end I was left with 17 of the "top" peer-review general science and medical/biomedical publications that had both a Facebook page and a Twitter feed:

Nature, PNAS, Science, The New England Journal of Medicine, Cell, The Lancet, Journal of the American Medical Association, British Medical Journal, PLoS Biology, PLoS Medicine, Genes & Development, Nature Medicine, Genome Research, The Journal of Experimental Biology, and Cell: Stem Cell

For each of these journals I then noted the number of "likes" on its Facebook page, which is a measure of how many people will see an announcement made by that journal. I also took note of how many Twitter followers each journal has, as well as how many people the journal follows and how many tweets per day the account makes, on average.

First, some simple metrics:
* Nature has received the most total cites with 511145
* The New England Journal of Medicine had the highest 2008-2010 impact factor at 53.5
* They have--by far--the most Facebook likes with 232385
* They also have the most Twitter followers with 31863
* The British Medical Journal has made the most tweets with 5405
* They follow the most twitterers with 1471
* And they are the most chatty with 5.4 tweets per day

First-pass metrics show that there is a strong correlation between number of tweets and number of followers (r = 0.63, p = 0.012) as well as the number of followers and tweets per day (r = 0.54, p = 0.037).

Tweet more, you get more followers.

(It's important to note that all metrics are on a log scale!)

Interestingly, total citations and impact factor are only weakly correlated (r = 0.49, p = 0.063).

The question is, do social media metrics explain any of the variance in citations or impact factor?

Again, looking at simple correlations, we see that number of Facebook page likes for a journal and the number of twitter followers it has are correlated (r = 0.53, p = 0.044). This probably represents measure of social networking engagement.

But what's crazy is that number of Facebook page likes is strongly correlated with the total number of citations a journal has received (r = 0.78, p = 0.001)!

Both Facebook page likes and number of Twitter followers correlate (equally well!) with impact factor (r = 0.59, p = 0.021; r = 0.59, p = 0.021 respectively).

For those of you who like a little more scientific rigor than a bunch of uncorrected correlations, I also ran a multiple (log-transformed) linear regression for total citations and impact factor separately. What's interesting is that, in both cases, number of Facebook page likes seems to be the dominant significant factor in determining citations and impact factor.

However, for the impact factor analysis, both the number of people the journal follows on twitter, as well as the number of tweets per day, are inversely correlated with impact factor (partial correlations of r = -0.44 and r = -0.66, respectively)!

So what does all of this mean?

Well, it seems like having a social media presence is probably a reflection of the journal's popularity in general, but that, on average, the journals that do the most social media engagement (amongst the top-tier journals!) show the lowest impact factors.

That's a little disheartening.

Why Netflixs' price hike is a brilliant move

2011-07-13T12:05:00.000-07:00

Why Netflixs' price hike is a brilliant move

Yesterday I--and millions of other Netflix customers--received an email similar to the one below:

This email states clearly that beginning 2011 Sep 1 Netflix will not longer have a DVD/streaming bundle, but rather begin charging separate fees for each service. Now, most people interpreted this as a major price hike and a "bonehead" move on the part of Netflix.

Here, I argue that not only was this a brilliant move on Netflix's part, but that ultimately that it will be better for all of us, their customers, leading to MORE streaming content.

In fact, if I worked for Netflix, I would have advised this move 12-24 months ago. I'm surprised they waited this long. (My science and analytics consulting fees are steep.)

The only ones who should be worried about this are the USPS.

You see, according to Netflix CEO Reed Hastings over on Quora, Netflix spends $500M - $600M per year on postage. This is a huge cost of doing business, and this is what I'm sure is driving this decision.

What follows is what I believe to be the most likely process that lead Netflix to this decision. I will make several assumptions, but if I were involved in Netflix these assumptions would have been corroborated by exact metrics and market testing. This will be back-of-the-envelope math, but I could easily run some simulations to show that for any given range of realistic values for each of my assumed variables this is still a good move.

First, assume a spherical cow that this move will cause several customers to abandon Netflix altogether out of some consumer rage . Let's assume 10%. This will roughly equal a loss in revenue equal to the average revenue per user times 10% of total users.

Next, there will be some proportion of users with streaming who will bite the bullet and pay the extra $10/month for a DVD. Let's assume this is much less than the proportion of users who leave, so that we go in with a "more worse" scenario. This seems more likely to me and, in fact, this won't drive

Finally, there will be many users with streaming who will say "F you Netflix I'm not paying an extra $10/month for one DVD!" (See Louis CK video)

This again represents a potentially huge loss in revenue. But it's a much BETTER gain for Netflix in that they don't have to pay all that damned postage!

Let's say that the difference between the proportion of users who pay the extra $10 for the DVD and those who leave represents a $100 MILLION annual loss in revenue. On the surface, this looks awful. (And I'm sure it can't possibly be even this much, but we're going worst-case here).

But then let's say that a massive proportion of users (smartly) drop the DVD option and move over to streaming-only, which is what I'm sure Netflix wants. Let's say 75% of users are reasonable and choose this option.

This means that cost of postage for Netflix drops to only $125-$150M per year. This represents a SAVINGS of at least $375M annually. Removing the $100M/year lost revenue from users who cancel, this still nets Netflix $275M annually.

Now Netflix could rest happily and stash this $275M/year. But what I guarantee they will do instead is use that huge amount of in-pocket savings to leverage distributors to allow them to stream more content.

And extra couple hundred million a year can go a looooooong way.

So yes, on the surface, this move seems to suck for us, the consumers. The streaming content sucks. It's spotty. But in the LONG RUN Netflix will be in a much better position to afford to stream more content.

Which is really what all of us want.

Working memory and cognitive enhancement

2011-07-12T13:48:00.000-07:00

Quora sucked me in again this weekend... I wrote three long answers over there to the following questions:

Maybe you can spot how all three questions are related.

The first question was the one I spent the most time on, as I covered a fair amount of he literature. I'm going to quote a lot of my answers here (since Quora lets you keep copyright on your writing there).

What is the most effective way to enhance working memory?

While it sucks to say it, there is no clear "most effective" way to enhance working memory, but the methods that have shown success are:

brain training
medication
neocortical stimulation

But for now, I'm sad to say, nothing's gonna turn you into Eddie Morra from Limitless quite yet...

For details and controversy, read on.

First, a big disclaimer: in my research I've published work looking into the neuroanatomical basis for visual working memory (Voytek & Knight, Prefrontal cortex and basal ganglia contributions to visual working memory, PNAS 2010 [open access]). This is a very complex field, because "working memory" isn't one single process controlled by one brain region, but it does appear to be critically reliant on the dorsolateral prefrontal cortex, among others (see: What are the primary functions of the dorsolateral prefrontal cortex?).

It's also intricately linked to attention and other cognitive processes (very roughly, see Voytek et al., Dynamic Neuroplasticity after Human Prefrontal Cortex Damage, Neuron 2010). Check out the relationships to different cognitive tasks and working memory according to brainSCANr:

The task referred to in the question, the n-back task, is a type of serial working memory task wherein a person must hold a series of information in memory. The simplest version of the task, the 0-back, requires the person to respond every time they see the target stimulus. At 2-back, the task becomes very difficult. In the 2-back version below, for example, correct responses would be to the second and third Cs, because in both cases there was a C 2-letters prior.

If presented with the following letters:
A D E Q E X S C E C T M T P W

then correct responses would be for the letters in bold:
A D E Q E X S C E C T M T P W

This is but one of many forms of experimentally testing working memory.

BRAIN TRAINING
There are several online systems for brain training, which aim to enhance cognitive performance (including working memory), such as Lumosity and Posit Science.

(See my answer to Does memory improvement software work?)

Some research has shown that fluid intelligence (which is a catch-all term) can be improved with working memory training (Improving fluid intelligence with training on working memory, PNAS 2008):

Fluid intelligence (Gf) refers to the ability to reason and to solve new problems independently of previously acquired knowledge. Gf is critical for a wide variety of cognitive tasks, and it is considered one of the most important factors in learning... Although performance on tests of Gf can be improved through direct practice on the tests themselves, there is no evidence that training on any other regimen yields increased Gf in adults. Furthermore, there is a long history of research into cognitive training showing that, although performance on trained tasks can increase dramatically, transfer of this learning to other tasks remains poor. Here, we present evidence for transfer from training on a demanding working memory task to measures of Gf. This transfer results even though the trained task is entirely different from the intelligence test itself. Furthermore, we demonstrate that the extent of gain in intelligence critically depends on the amount of training: the more training, the more improvement in Gf. That is, the training effect is dosage-dependent. Thus, in contrast to many previous studies, we conclude that it is possible to improve Gf without practicing the testing tasks themselves, opening a wide range of applications.

This issue of transfer is important, because it's easy to show that training someone on a working memory task can improve performance on that task, but does that improvement generalize to other aspects of cognition?

When you ask "What is the most effective way to enhance working memory?" you don't really care about just improving working memory. You want to be smarter all around!

Given that things such as attention and working memory are so intimately related, we would think that training would transfer, but the evidence is still quite murky.

For example, last year there was a big study that got a lot of coverage (Putting brain training to the test, Nature 2010) that found that:

‘Brain training’, or the goal of improved cognitive function through the regular use of computerized tests, is a multimillion-pound industry, yet in our view scientific evidence to support its efficacy is lacking. Modest effects have been reported in some studies of older individuals and preschool children, and video-game players outperform non-players on some tests of visual attention5. However, the widely held belief that commercially available computerized brain-training programs improve general cognitive function in the wider population in our opinion lacks empirical support. The central question is not whether performance on cognitive tests can be improved by training, but rather, whether those benefits transfer to other untrained tasks or lead to any general improvement in the level of cognitive functioning. Here we report the results of a six-week online study in which 11,430 participants trained several times each week on cognitive tasks designed to improve reasoning, memory, planning, visuospatial skills and attention. Although improvements were observed in every one of the cognitive tasks that were trained, no evidence was found for transfer effects to untrained tasks, even when those tasks were cognitively closely related.

(emphasis mine)

Contrast this with a review from this year (Does working memory training work? The promise and challenges of enhancing cognition by training working memory. Psychon Bull Rev 2011) that broke training into strategy and core training:

Strategy training paradigms involve teaching of effective approaches to encoding, maintenance, and/or retrieval from WM. The primary aim of most strategy training studies is to increase performance in tasks requiring retention of information over a delay. In strategy training studies, experimenters introduce participants to particular task strategies, and then provide practice sessions encouraging the strategy of interest. Some strategy training programs aim to increase reliance on, and facility with, articulatory rehearsal,while other programs aim to train elaborative encoding strategies...

Core training studies typically involve repetition of demanding WM tasks that are designed to target domain-general WM mechanisms. To achieve this purpose, core training paradigms are commonly designed to: 1) limit the use of domain-specific strategies, 2) minimize automization, 3) include tasks/stimuli that span multiple modalities, 4) require maintenance in the face of interference, 5) enforce rapid WM encoding and retrieval demands, 6) adapt to participants’ varying level of proficiency, and 7) demand high cognitive workloads or high intensity cognitive engagement (though different studies place variable emphasis on these factors). Tasks utilized in core training programs also commonly involve sequential processing and frequent memory updating.

The authors conclude:

In particular, core WM training studies seem to produce more far-reaching transfer effects, likely because they target domain-general mechanisms of WM. The results of individual studies encourage optimism regarding the value ofWM training as a tool for general cognitive enhancement.However, we discuss several limitations that should be addressed before the field endorses the value of this approach.

MEDICATION
The issue of using medication for cognitive enhancement is very contentious, however I will not discuss the ethics here.

In 2008, Nature ran a commentary on this topic: Towards responsible use of cognitive-enhancing drugs by the healthy in which the authors outline the evidence in favor of the efficacy of "smart drugs" (nootropics):

Many of the medications used to treat psychiatric and neurological conditions also improve the performance of the healthy. The drugs most commonly used for cognitive enhancement at present are stimulants, namely Ritalin (methyphenidate) and Adderall (mixed amphetamine salts), and are prescribed mainly for the treatment of attention deficit hyperactivity disorder (ADHD). Because of their effects on the catecholamine system, these drugs increase executive functions in patients and most healthy normal people, improving their abilities to focus their attention, manipulate information in working memory and flexibly control their responses...
A newer drug, modafinil (Provigil), has also shown enhancement potential. Modafinil is approved for the treatment of fatigue caused by narcolepsy, sleep apnoea and shift-work sleep disorder. It is currently prescribed off label for a wide range of neuropsychiatric and other medical conditions involving fatigue as well as for healthy people who need to stay alert and awake when sleep deprived, such as physicians on night call. In addition, laboratory studies have shown that modafinil enhances aspects of executive function in rested healthy adults, particularly inhibitory control. Unlike Adderall and Ritalin, however, modafinil prescriptions are not common, and the drug is consequently rare on the college black market. But anecdotal evidence and a readers' survey both suggest that adults sometimes obtain modafinil from their physicians or online for enhancement purposes.
A modest degree of memory enhancement is possible with the ADHD medications just mentioned as well as with medications developed for the treatment of Alzheimer's disease such as Aricept (donepezil), which raise levels of acetylcholine in the brain. Several other compounds with different pharmacological actions are in early clinical trials, having shown positive effects on memory in healthy research subjects.
It is too early to know whether any of these new drugs will be proven safe and effective, but if one is it will surely be sought by healthy middle-aged and elderly people contending with normal age-related memory decline, as well as by people of all ages preparing for academic or licensure examinations.

(emphasis mine)

Regarding the last class of drugs--the cholinergic drugs--my friend Ariel Rokem published research last year on the effect of Aricept on visual perceptual learning (Cholinergic enhancement augments magnitude and specificity of visual perceptual learning in healthy humans, Curr Biol 2010):

Acetylcholine (ACh) has been suggested to regulate learning by enhancing the responses of sensory cortical neurons to behaviorally relevant stimuli. In this study, we increased synaptic levels of ACh in the brains of healthy human subjects with the cholinesterase inhibitor donepezil (trade name: Aricept) and measured the effects of this cholinergic enhancement on visual perceptual learning. Each subject completed two 5 day courses of training on a motion direction discrimination task, once while ingesting 5 mg of donepezil before every training session and once while placebo was administered. We found that cholinergic enhancement augmented perceptual learning for stimuli having the same direction of motion and visual field location used during training. In addition, perceptual learning with donepezil was more selective to the trained direction of motion and visual field location. These results, combined with previous studies demonstrating an increase in neuronal selectivity following cholinergic enhancement, suggest a possible mechanism by which ACh augments neural plasticity by directing activity to populations of neurons that encode behaviorally relevant stimulus features.

(emphasis mine)

But again, remember the caveats about transfer in training: just because a drug enhances one aspect of cognition (visual perceptual learning) does not mean it will transfer to others (e.g. working memory).

Just this year, a study in Nature (A critical role for IGF-II in memory consolidation and enhancement, 2011) showed that another type of drug, insulin-like growth factor II, enhances memory in rats:

We report that, in the rat, administering insulin-like growth factor II (IGF-II, also known as IGF2) significantly enhances memory retention and prevents forgetting. Inhibitory avoidance learning leads to an increase in hippocampal expression of IGF-II, which requires the transcription factor CCAAT enhancer binding protein β and is essential for memory consolidation. Furthermore, injections of recombinant IGF-II into the hippocampus after either training or memory retrieval significantly enhance memory retention and prevent forgetting. To be effective, IGF-II needs to be administered within a sensitive period of memory consolidation. IGF-II-dependent memory enhancement requires IGF-II receptors, new protein synthesis, the function of activity-regulated cytoskeletal-associated protein and glycogen-synthase kinase 3 (GSK3). Moreover, it correlates with a significant activation of synaptic GSK3β and increased expression of GluR1 (also known as GRIA1) α-amino-3-hydroxy-5-methyl-4-isoxasolepropionic acid receptor subunits. In hippocampal slices, IGF-II promotes IGF-II receptor-dependent, persistent long-term potentiation after weak synaptic stimulation. Thus, IGF-II may represent a novel target for cognitive enhancement therapies.

BRAIN STIMULATION
This is seriously DO NOT TRY THIS AT HOME territory.

DO NOT TRY THIS AT HOME

But this year, a cool study was published in Clinical Neurophysiology (Improving working memory: Exploring the effect of transcranial random noise stimulation and transcranial direct current stimulation on the dorsolateral prefrontal cortex, 2011) showing that transcranial direct current stimulation (tDCS) of the dorsolateral prefrontal cortex (a brain region known to be critical for maintaining items in working memory) may enhance working memory. tDCS is a simple system wherein a low, direct current is passed between two electrodes on the scalp, inducing a current between them intracerebrally. The researchers report that:

There was significant improvement in speed of performance following anodal tDCS on the 2-back WM task; this was the only significant finding... The results do not provide support for the hypothesis that tRNS improves WM. However, the study does provide confirmation of previous findings that anodal tDCS enhances some aspects of DLPFC functioning. Methodological limitations that may have contributed to the lack of significant findings following tRNS are discussed.

Does memory improvement software work?Short answer: yes. Real answer: it depends on what you mean by "works".

I go into a lot of details about current neuroscientific methods used to try and improve cognitive functions over on my answer to What is the most effective way to enhance working memory?There are a lot of brain training games and software out there: Brain Age, Lumosity, Posit Science, etc.Basically, the research is really murky. It's pretty clear that you can train someone on one aspect of cognition, like working memory, and improve their working memory. What is less clear is whether that training transfers to other aspects of cognition.So if I train your working memory, are you faster at noticing brief visual stimuli (can you play Halo better?) Can you pay Attention longer? How long does this training last. Has the training made you "smarter", or is it just "teaching to the test"?Some research has shown that fluid intelligence (which is a catch-all term) can be improved with working memory training (Improving fluid intelligence with training on working memory, PNAS 2008):

Fluid intelligence (Gf) refers to the ability to reason and to solve new problems independently of previously acquired knowledge. Gf is critical for a wide variety of cognitive tasks, and it is considered one of the most important factors in learning... Although performance on tests of Gf can be improved through direct practice on the tests themselves, there is no evidence that training on any other regimen yields increased Gf in adults. Furthermore, there is a long history of research into cognitive training showing that, although performance on trained tasks can increase dramatically, transfer of this learning to other tasks remains poor. Here, we present evidence for transfer from training on a demanding working memory task to measures of Gf. This transfer results even though the trained task is entirely different from the intelligence test itself. Furthermore, we demonstrate that the extent of gain in intelligence critically depends on the amount of training: the more training, the more improvement in Gf. That is, the training effect is dosage-dependent. Thus, in contrast to many previous studies, we conclude that it is possible to improve Gf without practicing the testing tasks themselves, opening a wide range of applications.

Now, we know that general features of cognition "share" the same brain areas. That is, damage to various parts of the prefrontal cortex leads to impairments to working memory, attention, fluid reasoning, set-shifting, emotional regulation, and so on.Given that things such as attention and working memory are so intimately related (both neuroanatomically and psychologically), we would think that training would transfer, but that doesn't necessarily seem to be the case.See Putting brain training to the test and the associated controversy again.So yes, training "works" in the sense that you'll get better at the task, but it may not make you "smarter" overall.What are the primary functions of the dorsolateral prefrontal cortex? The dorsolateral prefrontal cortex (dlPFC) is a region in the frontal lobes toward the top and side: hence dorso (top) and lateral (side).

There's a very rich history of research about this brain region. However I do a lot of work in this area, so I'll stick to talking about this brain region, as well as a give a general overview.First, the anatomy: the dlPFC is a neocortical brain region, meaning it is part of the outer "cortex" (Latin: "bark" or "rind") of the brain. More generally, it's part of the "prefrontal cortex", which are the brain regions anterior (forward) from the motor parts of the frontal lobes:

It is heavily interconnected with a variety of other cortical brain regions, sending and receiving inputs to/from most sensory brain regions, as well as subcortical brain regions like the basal ganglia:

That figure above is from one of my research papers (Voytek & Knight, Prefrontal cortex and basal ganglia contributions to visual working memory, PNAS 2010 [open access]). In it, I was examining the differential effects of dlPFC or basal ganglia brain lesions on working memory performance, and argue that while the dlPFC plays an important role in complex cognition, ultimately it is the coordinated action between clusters of brain regions that gives rise to it.(For a quick primer on working memory, see my answer to: What is the most effective way to enhance working memory?)Working memory is a cognitive function known to be dependent on the dlPFC. You see, we have two basic ways of showing how a brain region does anything:

Correlate brain activity as measured with imaging techniques like fMRI or PET, or with electrodes implanted into single neurons or neuronal groups, with some behavior like working memory; or,
See how damage to a brain region effects behavior.

(Through clever use of behavioral experimentation that is designed to target certain aspects of neuroanatomy, you can also gain a lot of novel brain-based information.)Note there are many caveats (see my answer to What is the neurological basis of curiosity? or my post How to be a neuroscientist)But basically, these are the methods used in modern neuroscience, and how we know what the function of any brain region is.I try and combine all of the above methods in my research by using crude neuroimaging (EEG) and working with people who have had brain lesions (such as caused by stroke) restricted to a specific area (such as the dlPFC) while they perform a carefully-designed behavioral experiment.Here's a quick overview of how the dlPFC relates to topics in the peer-reviewed literature, according to brainSCANr:

You can see it relates to a lot of brain regions (yellow) and strongly to a few cognitive functions (red). Importantly, the dlPFC relates to "executive functions", a catch-all term for a cluster of higher cognitive skills, such as:

working memory maintenance
attention

set-shifting (update a behavior when the rules change on you)

reward evaluation

motor planning

Research with such patients has shown that damage to the dlPFC causes deficits in these skills, as well as issues with motor planning, social cognition, and even multi-sensory integration. Neuroimaging studies corroborate these associations between the dlPFC and behavior. Voytek B, & Knight RT (2010). Prefrontal cortex and basal ganglia contributions to visual working memory. Proceedings of the National Academy of Sciences of the United States of America, 107 (42), 18167-72 PMID: 20921401 Voytek B, Davis M, Yago E, Barceló F, Vogel EK, & Knight RT (2010). Dynamic neuroplasticity after human prefrontal cortex damage. Neuron, 68 (3), 401-8 PMID: 21040843 Jaeggi SM, Buschkuehl M, Jonides J, & Perrig WJ (2008). Improving fluid intelligence with training on working memory. Proceedings of the National Academy of Sciences of the United States of America, 105 (19), 6829-33 PMID: 18443283 Owen AM, Hampshire A, Grahn JA, Stenton R, Dajani S, Burns AS, Howard RJ, & Ballard CG (2010). Putting brain training to the test. Nature, 465 (7299), 775-8 PMID: 20407435 Morrison AB, & Chein JM (2011). Does working memory training work? The promise and challenges of enhancing cognition by training working memory. Psychonomic bulletin & review, 18 (1), 46-60 PMID: 21327348 Greely H, Sahakian B, Harris J, Kessler RC, Gazzaniga M, Campbell P, & Farah MJ (2008). Towards responsible use of cognitive-enhancing drugs by the healthy. Nature, 456 (7223), 702-5 PMID: 19060880 Rokem A, & Silver MA (2010). Cholinergic enhancement augments magnitude and specificity of visual perceptual learning in healthy humans. Current biology : CB, 20 (19), 1723-8 PMID: 20850321 Chen DY, Stern SA, Garcia-Osta A, Saunier-Rebori B, Pollonini G, Bambah-Mukku D, Blitzer RD, & Alberini CM (2011). A critical role for IGF-II in memory consolidation and enhancement. Nature, 469 (7331), 491-7 PMID: 21270887 Mulquiney PG, Hoy KE, Daskalakis ZJ, & Fitzgerald PB (2011). Improving working memory: Exploring the effect of transcranial random noise stimulation and transcranial direct current stimulation on the dorsolateral prefrontal cortex. Clinical neurophysiology : official journal of the International Federation of Clinical Neurophysiology PMID: 21665534 Jaeggi SM, Buschkuehl M, Jonides J, & Perrig WJ (2008). Improving fluid intelligence with training on working memory. Proceedings of the National Academy of Sciences of the United States of America, 105 (19), 6829-33 PMID: 18443283

The top 11 (or 23) unanswered questions in neuroscience

2011-07-06T09:09:00.000-07:00

This post has been in my draft for a while, and recently it came up as a question over at Quora, so I finally got around to finishing it.

What are the really big questions right now in neuroscience?

This is a fun game that a lot of neuroscientists like to play (usually over a few drinks). Generally our responses fall under one of two categories (of which I'd argue all others are just more detailed sub-questions). They are:

Consciousness WTF!?
How can atoms and molecules combine to a behaving animal?

When I was first starting my PhD there was a series of book chapter PDFs that were getting passed around from a book co-authored and edited by David Eagleman and Patricia Churchland that was supposedly going to be published in 2006 titled, Ten Unsolved Questions of Neuroscience.

As far as I can tell, that book never saw print, though you can find the draft chapters online in that link above. The authors of the chapters in that non-book are an excellent selection of outstanding neuroscientists from 2006.

In 2007, Eagleman basically turned what I assume was the book outline into a short essay in Discover titled "10 unsolved mysteries of the brain".

The list from his Discover piece differs slightly from the 10 chapters of the book:

How is information coded in neural activity?
How are memories stored and retrieved?
What does the baseline activity in the brain represent?
How do brains simulate the future?
What are emotions?
What is intelligence?
How is time represented in the brain?
Why do brains sleep and dream?
How do the specialized systems of the brain integrate with one another?
What is consciousness?

The following question was not in the Discover piece, but is in the book draft:

How do brains balance plasticity against retention?

It's this last one that I find the most fascinating. So much so, that the (PDF) opening line of my PhD thesis is:

How do we maintain a stable percept of the world in the face of the powerful drive of neuroplasticity in both health and disease?

(If you've read any of my research, this should be no surprise.)

Now, it seems that the woo woo crowds (and bad science journalists) have a tendency to pull out the word neuroplasticity about as readily as they will the word quantum when "explaining" certain nebulous phenomena. This is so common that "neuroplasticity" is becoming a dirty word.

Yet, as Micah Allen pointed out last night:

I find it funny in the space of 10 years we've gone from excited about neuroplasticity to totally cynical. I'm an anti-cynic.less than a minute ago via TweetDeck Favorite Retweet ReplyMicah Allen
neuroconscience

Hype sucks, but let's not go back to the days when neurologists refused to treat patients because "the brain isn't plastic."less than a minute ago via TweetDeck Favorite Retweet ReplyMicah Allen
neuroconscience

I find it interesting that Eagleman chose to replace the question about neuroplasticity with the question about consciousness for the Discover piece.

You know you're in bad shape when consciousness seems to be the more reasonable alternative.

Jordan Grafman has a fun, short article published in Brain and Cognition in 2000 titled, Picking Two Scientific Roses for the Next Century. In that, he highlights neuroplasticity as a major research endeavor, but he breaks it down more scientifically:

"Neuroplasticity has at least four distinctive expressions:

(1) Flexibility of local cortical (representational) maps to expand and contract and to store new items;
(2) Homologous region adaptation—-for example, when brain damage affects the left parietal lobe, can the right parietal lobe reorganize itself to allow the representation of forms of information previously stored in the left parietal lobe?
(3) Sensory substitution where one cortical area previously committed to processing information in one sensory domain (e.g., vision) adapts to input from a different sensory domain (e.g., touch);
(4) Compensatory reorganization where the remaining components of a configured cognitive process perform well enough so that the person can achieve the desired performance outcome (even if it is now accomplished somewhat differently than before)."

A ton of exciting research has been done on these questions since that writing.

In addition to the Eagleman list, there's a more specifically detailed list from a book edited by J. Leo van Hemmen and Terry Sejnowski called (PDF) 23 Problems in Systems Neuroscience which was published in 2006 by Oxford University Press.

While there is certainly overlap with the Eagleman questions, the van Hemmen/Sejnowski list includes more biologically-specific, "lower-level" questions, as opposed to Eagleman's "higher-level" conceptual questions:

Shall We Even Understand the Fly's Brain?
Can We Understand the Action of Brains in Natural Environments?
Hemisphere Dominance of Brain Function--Which Functions Are Lateralized and Why?
What Is the Function of the Thalamus?
What Is a Neuronal Map, How Does It Arise, and What Is It Good For?
What Is Fed Back?
How Can the Brain Be So Fast?
What Is the Neural Code?
Are Single Cortical Neurons Soloists or Are They Obedient Members of a Huge Orchestra?
What Is the Other 85 Percent of V1 Doing?
Which Computation Runs in Visual Cortical Columns?
Are Neurons Adapted for Specific Computations?
How Is Time Represented in the Brain?
How General Are Neural Codes in Sensory Systems?
How Does the Hearing System Perform Auditory Scene Analysis?
How Does Our Visual System Achieve Shift and Size Invariance?
What Is Reflected in Sensory Neocortical Activity: External Stimuli or What the Cortex Does with Them?
Do Perception and Action Result from Different Brain Circuits?
What Are the Projective Fields of Cortical Neurons?
How Are the Features of Objects Integrated into Perceptual Wholes That Are Selected by Attention?
Where Are the Switches on This Thing?
Synesthesia: What Does It Tell Us about the Emergence of Qualia, Metaphor, Abstract Thought, and Language?
What Are the Neuronal Correlates of Consciousness?

This is a great list because the problems are (generally) better defined and seem more tractable. But it's less fun for the same reason!

There are dozens of paper citations I'd love to add here to complement that list, but that would take forever. So if you're more interested in any specific topic, shoot me a message in the comments and I'll try and point you to some of my favorite references.

Grafman, J. (2000). Picking Two Scientific Roses for the Next Century Brain and Cognition, 42 (1), 10-12 DOI: 10.1006/brcg.1999.1147
Voytek B, Davis M, Yago E, Barceló F, Vogel EK, & Knight RT (2010). Dynamic neuroplasticity after human prefrontal cortex damage. Neuron, 68 (3), 401-8 PMID: 21040843
Sadato N, Pascual-Leone A, Grafman J, Ibañez V, Deiber MP, Dold G, & Hallett M (1996). Activation of the primary visual cortex by Braille reading in blind subjects. Nature, 380 (6574), 526-8 PMID: 8606771

Using Science to Survive the Zombie Apocalypse

2011-06-30T15:34:00.000-07:00

Man, I wish my real neuroscience research got as much attention as my fake science! What does that say about my quality of work, eh? :D

So once again serendipity has reared its lovely head. Actually, that's unfair, I wouldn't call what's happened here "luck", as there's been a lot of leg-work and networking that gotten this stuff out there, but anyway...

A few weeks ago I answered a question on Quora: What are some ways to survive the Zombie Apocalypse?

I filled it with tons of pictures that Tim Verstynen and I made as part of our work with the Zombie Research Society for zomBcon last year (where I got to meet and interview George Romero!)

In that answer I linked to my NerdNite presentation that had tons of those "data":

Nerd Nite SF: "Scanning the Zombie Brain" by Dr. Bradley Voytek, 1/19/11 from nerdniteSF on Vimeo.

Well, someone working with Pimsleur saw the video and Quora response and shot me an email asking if he could create an infographic on how our "results" inform ways in which we could survive the zombie apocalypse.

In the mean time I'd been in touch with Angela over at Wired about doing something zombie-related, and this seemed like the perfect opportunity.

She thought so too! So here's the article on Wired:

How to Survive the Zombie Apocalypse Using Science

I've talked at length on this blog about why I do the zombie neuroscience stuff: it's a tongue-in-cheek jab at cognitive neuroscience, it gets people to accidentally learn about the brain, and it's just damn excellent geeky fun!

So far this zombie stuff has lead to an interview for National Geographic's The Truth Behind Zombies, my new article in Wired, speaking at zomBcon, and now speaking on two panels at Comic-Con.

Like I said, if only my actual research lead to such opportunities!

brainSCANr at the Human Brain Mapping conference!

2011-06-29T06:16:00.000-07:00

Just a quick note: I'm up in Quebec City for the 17th annual Organization for Human Brian Mapping conference (OHBM, or just "HBM"). This is my first time at this conference, since it's usually considered to be an (f)MRI conference, which isn't really my thing.

I'm much more of an EEG/ECoG researcher (see my PNAS, Neuron, Frontiers in Human Neuroscience, and Journal of Cognitive Neuroscience papers).

However, I'm here to present some of the latest work on brainSCANr.

Speaking of brainSCANr, Tal Yarkoni just released the public beta version of his neuroimaging meta-analytics tool, neurosynth just in time for OHBM! It's an amazing piece of technology recently published in Nature Methods, so you should check it out.

Also, this conference is my wife Jessica's first publication at a scientific meeting, so please everyone give her a round of applause! She did all of the system design, visualization, etc. for brainSCANr.

We've delayed the paper to work on what I'm calling "semi-automated hypothesis generation". We've also been working on integrating our findings with gene expression data from the Allen Brian Atlas (ABA).

So I spilled the beans on Quora last week about what we've been up to on brainSCANr. Someone asked a series of brainSCANr questions that I answered. It was pretty cool to see then on there actually. I was pleased!

* How are brainSCANr and the Allen Brain Atlas similar; how are they different?
* What discoveries or insights have come out of brainSCANr?
* What data analysis and visualization technologies underlie brainSCANr?

In one of my responses on Quora, I explain the hypothesis generation method a bit:

Note this is preliminary, but the idea is to find associations that are disproportionally ranked to find possible missing research associations. In the example above, for instance, "migraine" is most strongly associated with "serotonin", but "serotonin" is relatively weakly associated with "migraine" compared to how much more strongly it's associated with other terms such as the raphe nuclei, anxiety, etc. By using this calculation metric, we are attempting to find "holes" in the scientific literature, and trying to infer possible new or under-studied paths of research.

I also explain the integration with the ABA:

In the image above, you can see the actual gene expression profile for a serotonin receptor gene (HTR1A). As expected, this gene has a very high expression profile in the raphe nuclei, which brainSCANr tells us is the brain region most strongly associated with serotonin.

Interestingly, however, the raphe nuclei are not the brain region that most strongly expresses the HTR1A gene. In fact, the region that does so is the zona incerta, a brain region that is very weakly associated with serotonin.

In fact, at the time of this writing, the zona incerta has two orders of magnitude fewer co-papers with serotonin than do the raphe nuclei (42 papers versus 4482).

This suggests that there is an overemphasis in the literature on the raphe nuclei and serotonin, and a serious dearth of information about the zona incerta.

We believe the combined information between the ABA and brainSCANr will offer some exciting insights.

Anyway, if you're at the conference, come drop by my poster on Wednesday or Thursday. I'll be in front of the poster from 10:30am onward Thursday morning, but sadly, due to the fact that she's 30-something weeks pregnant, my wife couldn't make the fight out to present with me.

This post is getting long, so I'll cut short my thoughts on Quebec and just post a few pictures and a video. The video is from the amazing (and free!) Cirque du Soleil show, Les Chemins Invisibles. This show is performed outside under a highway overpas for free during the summer in Quebec City. Incredible.

My plane from Montreal to Quebec was super tiny. May have been the smallest plane I've been on:

The conference has a cool art section that I'm really happy to see:

And the old city itself is very cool... feels very Victorian European:

But the street art reminds you that you're not living in 1850:

Thankfully, I've found a nice place to spend my evenings:

My Scientific American post: "What bats, bombs, and sharks taught us about hearing"

2011-06-14T08:43:00.000-07:00

A few weeks ago I was asked by the man himself, Bora Zivkovic of the Scientific American blog, if I wanted to write a guest post.

There was one I'd been wanting to write for a while but hadn't gotten around to because of the amount of work that it would require. Well I finally got around to it, and it's posted over on SciAm. It's the most proper "news article-like" thing I've written.

Please give it a read!

What bats, bombs, and sharks taught us about hearing

(Robert Galambos, MD, PhD - Source: New York Times)

The post is about my great-grand advisor, Robert Galambos, the man who discovered, among several other cool things, that bats use echolocation to navigate.

(Bat echolocation - Source: ASU School of Life Sciences: Ask a Biologist)

I also uploaded a video of his original echolocation experiments from 1940:

I had to edit out a few pieces of the video from the original Galambos version, but I honestly didn't cut anything critical. I left in all of his narration. The only parts I cut were the repetitions showing the bats flying normally, bats flying awkwardly, etc. He had several extra minutes of these segments to help demonstrate his point.

As for my article, I'd appreciate it if you all would read the whole thing, mainly because I'd love to get your feedback and thoughts on it!

Here's one of my favorite excerpts:

What impressed me the most about Galambos though wasn't his superb research, but rather the extent to which he'd sacrifice himself for his pursuit of knowledge.

I'm fascinated by the history of self-experimentation in neuroscience and medicine and have written about the topic previously. Sir Henry Head severed nerves in his own arm to document how sensation is regained after nerve damage. The history of endocrinology can be traced back to Dr. Brown-Séquard injecting himself with dog sperm to study its effect on his vitality and vigor...

In another experiment, conducted in response to the bombing of Pearl Harbor in 1942, Galambos and hearing researcher Hallowell "Hal" Davis were asked to "find out how much and what kind of sound it takes to injure or incapacitate a man."

How did they test this? Galambos explains:

we proceeded to expose our ears to the sound waves emitted by a so-called bullhorn, the kind of loudspeaker the Navy used to deliver messages to personnel wearing earplugs on the busy flight deck of an aircraft carrier. We systematically varied the three sound variables--intensity, frequency, and duration--producing in ourselves increasingly larger temporary hearing losses, until we neared combinations we thought might cause a permanent loss. At the end of the project, Hal decided to find out if our predictions were correct, and told us to expose his right ear--we always protected his left ear--to a wideband noise at 130 dB for 32 minutes. As predicted, this exposure permanently sliced a few hundred Hz off the high end of his existing congenital hearing loss in the 3500-3800 Hz region.

They partially deafened themselves. For science!

I'm excited about this piece, but it was a lot of work, so I don't think I'll be writing these kinds of pieces often.

I've got too much science to do!

A neuroscientist walks into a startup...

2011-06-09T14:30:00.000-07:00

It's been a hell of a few weeks! Beyond moving to a new house and starting a new job, I've had a lot of science going on.

A couple of weeks ago my off-the-cuff post "we are all inattentive superheroes" kinda... well... blew up, much to my surprise. It got picked up by BoingBoing, the Seattle PI, metafilter, Forbes' Robot Overlords blog, and many other places.

Since then I've been asked to write a post for the Scientific American guest blog. My post for that will go live next week (I'll post it here once it's up).

I've also joined The National Academy of Science's "Science & Entertainment Exchange" as a consultant, which may be pretty exciting.

Next, as part of my work with the Zombie Research Society, I'll be speaking on a panel called "History of the Modern Zombie" at this year's Comic-Con. I've been going to Comic-Con since I was about 12, so I'm really excited about being a part of this.

The other piece of big news is that my post-doctoral grant got funded, which means starting this Fall I will be employed at UCSF working in Adam Gazzaley's lab. This guarantees me three years of funding, which is great. I'm going to continue my research on the role that neuroplasticity plays in cognition. While I'd love to tell more, I'm being intentionally cagey about the details right now as we're already considering publishing a paper based on some of our results.

But it will be a few months before I start at UCSF, so I've got a few free months.

In the meantime I'll be working with one of my oldest friends, Curtis Chambers, at the startup where he works in San Francisco: Uber (New York Times coverage here and here; Wired here). In short, it's an on-demand car service where you reserve a black-car via an iPhone or Android app, or via SMS.

I'm working as their computational scientist (aka, "data pornographer") working on internal tools and analytics as well as writing a public-facing blog. Our goal is to use our historical data to more accurately estimate and reduce pick-up times.

I conceive of this as a Silicon Valley sabbatical, of sorts.

My first thought about making the academia > startup jump is best summed up by Dr. Ray Stantz:

For those of you who know me, or who saw my Google Tech Talk, you know how important a role I believe data will play in the future of science. Part of that will be sophisticated data mining and analytics, and that will be complemented by data visualization.

brainSCANr was my first attempt at bringing neuroscience into the data-driven future. By working closely with the tech community, I hope to gain new skills and connections that will help me go farther.

The data visualization and analysis I'm doing at Uber has been really fun; the data we're collecting here is huge. It's very data-driven. It's seriously impressive, and I think that neuroscientists (and academics in general) could learn a lot by interfacing with tech companies.

For example, check out the map I made of where all of our cars have been in San Francisco:

This past weekend my wife and I were driving around and I was geeking out about some of the analytics that we're working on at Uber. Her response was (to paraphrase), "it's amazing what happens when you put a bunch of nerds in a room together; somehow you guys are making getting a car to pick you up an interesting problem".

I'm used to working on problems deeply and slowly. That is, in academia we only publish when everything's in a relatively final form. The trick with a startup is rapid, incremental improvements. This is very different from academia (though I will gladly rant about how much I think academia could benefit from working with startups and data companies...)

More and more I have become interested in the data collection > analysis > visualization > interpretation workflow, and how technological improvements can help neuroscience research.

For the most part scientists and researchers, by definition, have very specific domain knowledge. But neuroscience in particular is a field that requires more knowledge than any one person can integrate: biology, chemistry, mathematics, philosophy, linguistics, psychology, and so on.

The farther along the field gets, the more tools will be required for data analysis and visualization of brain data. That is, the field badly needs maps and analytics tools. Statistics and programming are becoming critical components to assist in the neuroscience research process.

Which is exactly what I'm doing for Uber.

I'm building geo-location and analytics tools using python and js. It's amazing how much optimization and analysis can be done using the data we've collected. As Henry's post shows, every ride you take makes us smarter. Mapping the flow of a city like San Francisco or New York is amazing.

At the same time, I'm in an environment with amazing coders and thinkers, learning new tools that I can then turn around and apply to my research.

Exciting times.

Hey. Sup?

2011-05-16T09:21:00.000-07:00

So my last post drew a lot of new readers.

Because there are so many new people here, I'd like to play a couple of games.

The first I learned from Ed Yong:

1. Who are you?! Please leave a comment and tell me who you are and what your interest is in neuroscience (which is, I presume, why you're here). If you're a neuroscience student, tell me what you're studying!

The second is a game I first played on twitter a few months ago.

2. Ask me any neuro question and I'll try to answer it.

That one was fun, but it can take a while, since I try to support my answers with actual research. So bear with me!

For some reason my last post got passed around the internet a lot... with a strange phrase added to it in some places: "our senses would amaze us, if only we gave them our full attention, as animals do," which sounds a little... fluffy. I certainly didn't say that.

If you're expecting a blog by someone who would write something like that, I'm sorry to say you might be disappointed.

I tend to be a pretty hard skeptic. Especially so for neuroscience and my own work. Which isn't to say I don't sometimes do or say weird things. I just don't say weird things that sound like that.

Now I'd like to introduce myself a bit: I'm a neuroscience post-doc working at the University of California, Berkeley. In a few months I'm headed over to UCSF. This blog started as a way to write more openly about my own research and to share some of the analysis code I've written and projects I'm running.

For example, I run brainSCANr with my wife, Jessica Voytek, which is an experiment wherein we're quantifying connections between concepts in the neuroscience literature.

I'm also kinda known as the zombie neuroscience guy because of some of my public lecturing. But don't let that fool you. It's mainly a subversive way for me goof off while also trying to be more critical about neuroscience. This is a tough field, the problems we think about are difficult, and the media plays a strange role in feeding into some weird neuroscience myths.

To share some of my favorite posts, I'd like to point out "how to be a [critical] neuroscientist", which discusses how I do my first-pass read on cognitive neuroscience research, as well as "scientific acupuncture", which looks at media reporting on neuroscience.

There's also my general take on the whole media doc phenomenon:
(Click to enlarge)

I'm also partial to neuroscience history, because there are so many amazingly weird people involved. Check out "Sir Henry Head's self experimentation" or "Brown-Séquard, spinal cord research, and sperm injections".

Finally, the vanity part. I do talk about my own research. But the biggest motivation isn't vainglory, I swear. I'm a huge believer in the idea that, if I can't explain my research in a simple manner, it's because I don't actually know what I'm talking about. It's very easy to trick myself into believing that my over-education has taught me something, only to find that when I try to explain an idea simply all I'm actually doing is parroting back phrases that don't really mean anything.

So to avoid boring all my friends at the pub all the time, I use this blog to work out ideas. Here are my research posts:

Word.

We are all inattentive superheroes

2011-05-09T09:42:00.000-07:00

One of the more interesting parts about being a neuroscientist is when I'm suddenly struck by how absolutely weird our brains are.

And I'm not even talking about the super trippy stuff like free-will; even the mundane things are really mind-boggling.

For example: what does it mean to experience the world around us? We "see" things because photons that manage to pass through the inside-out design of our retinal cells cause a molecular change in the photoreceptors such that 11-cis-retinal isomerizes... etc.

(Tons of way overly detailed biology cut from here...)

When we "hear" things, the sound pressure waveform hits the tympanic membrane (eardrum) and ultimately causes the basilar membrane in your cochlea to vibrate. The basilar membrane is stiffer at one end (the basal end) and less stiff at the other end (the apical end). This fact was observed by Georg von Békésy (and earned him the 1961 Nobel Prize in Physiology or Medicine).

Here's a gratuitous, yet cool, video of this frequency decomposition in action:

Okay, great, so we know a ton of the basic biology and cellular mechanisms of the signal transduction mechanisms of our sensory apparatus.

But damn if I'm still not amazed by the actual experience of sensation.

Even beyond the philosophical wonder of passively sampling our outside environment in a shared, meaningful fashion is the ridiculous sensitivity of our senses.

We're used to thinking of our senses as being pretty shite: we can't see as well as eagles, we can't hear as well as bats, and we can't smell as well as dogs.

Or so we're used to thinking.

It turns out that humans can, in fact, detect as few as 2 photons entering the retina. Two. As in, one-plus-one.

It is often said that, under ideal conditions, a young, healthy person can see a candle flame from 30 miles away. That's like being able to see a candle in Times Square from Stamford, Connecticut. Or seeing a candle in Candlestick Park from Napa Valley.

Similarly, it appears that the limits to our threshold of hearing may actually be Brownian motion. That means that we can almost hear the random movements of atoms.

We can also smell as few as 30 molecules of certain substances.

I mean, we're talking serious Daredevil-level detection here!

(Frank Miller. Daredevil(c) Marvel Comics via Drawing Files)

These facts suggest that we all have some level of what we'd normally think of as "super human" sensory abilities already.

But what the hell? If I can supposedly see a candle from 30 miles away, why do I still crack my frakkin' shin on the coffee table when it's only slightly dark in my living room?

Well, for one thing, attention plays a very important role. For example, consider the very famous visual attention experiment below:

How can we see TWO PHOTONS, but miss THAT!?

The easy hypothesis? Attention.

You see, in the experiments testing the physical limits of the human sensory systems, the subjects involved are dedicating a lot of attention to the one sense being tested, almost certainly at the exclusion of the other senses.

I think we all have a pretty intuitive grasp of this. And sometimes our intuitive corrections are pretty damn funny. If you watch people's behavior carefully you'll notice some strange behaviors that we do.

Have you ever been driving around, trying to find a particular address, and then turn down the radio as you get close to where you think your destination is? Why would you turn down the radio when what you're doing is looking for an address? Seems pretty silly.

Do you close your eyes when you're trying to do calculations in your head? Why?

I think the answer to these questions is because we're trying to reduce sources of noise to maximize the amount of attention we can pay to the task at hand. The sounds from the radio capture your attention, making it hard to visually search for the address numbers on the house you're trying to find. Visual distractions in our surroundings may prevent us from maximally focusing our attention internally when trying to do hard math problems in our heads.

It strikes me that the experiments on the physical limits of our perception are probably also related to the adage that if you lose one sense, your remaining senses get heightened. This is a pretty common saying, but is it really true that if I became blind that I'd suddenly gain super-human hearing?

In a series of Nature studies published in the 1990s, it was shown that blind subjects reading via Braille actually use their visual cortex when reading by touch. This was demonstrated not only using brain imaging (PET, in this case), but also more causally via disruption of the visual cortex via TMS, a technique that can safely and reversibly disrupt the ability of a small region of the brain to process stimuli.

(See my basic primer on brain imaging techniques for a little more detail.)

When TMS was used to disrupt the visual cortex of blind subjects, their ability to read Braille characters dropped!

Anecdotally, the impressive sensory adaptations by blind people can be seen in two particularly striking subjects.

The first is a blind boy who was able to navigate so well via echolocating his own clicking sounds that he could ride a skateboard.

The second example is of another blind young man who was able to play video games by sound alone. The guy could track the sounds in a game and use them to play through to completion.

(That second story, by the way, would make for an amazing addition to the Serious Games Summit...)

In my own research I've tried to identify which regions of the brain are critical for attention and working memory, to understand how cognitive functions reorganize after brain damage, and to provide a physiological basis for how sensory and cognitive systems could interact.

In my future research I will further examine how sensory and cognitive systems interact and interrelate in more detail.

For now, sometimes the only thing I can do is sit back and marvel at how amazing it is that this three pounds of fat and water in my head does anything at all.
.
.
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(No matter how much beer I throw at it!)

Bialek, W. (1987). Physical Limits to Sensation and Perception Annual Review of Biophysics and Biophysical Chemistry, 16 (1), 455-478 DOI: 10.1146/annurev.bb.16.060187.002323
Sadato N, Pascual-Leone A, Grafman J, Ibañez V, Deiber MP, Dold G, & Hallett M (1996). Activation of the primary visual cortex by Braille reading in blind subjects. Nature, 380 (6574), 526-8 PMID: 8606771
Cohen LG, Celnik P, Pascual-Leone A, Corwell B, Falz L, Dambrosia J, Honda M, Sadato N, Gerloff C, Catalá MD, & Hallett M (1997). Functional relevance of cross-modal plasticity in blind humans. Nature, 389 (6647), 180-3 PMID: 9296495

Rectal ballon inflation

2011-05-06T11:51:00.000-07:00

In my previous neuroscience life I worked as a radioactive urine cleaner at UCLA.

The lab I worked in did some really cool research on the long-term neurological and behavioral effects of methamphetamine abuse. One of the researchers I worked with in that lab, Dr. Berman, was a great guy who had a pretty esoteric research specialty.

A few years ago he published an interesting, unique paper in The Journal of Neuroscience titled "Reduced brainstem inhibition during anticipated pelvic visceral pain correlates with enhanced brain response to the visceral stimulus in women with irritable bowel syndrome".

(CDC website woman indicating bowel discomfort)

Irritable bowel syndrome is an interesting condition which, according to wikipedia and its sources (I know... lazy me), has no clear organic cause, but definitely has a physical effect on sufferers. As Berman et al. say:

Symptom-related anxiety is a key predictor of IBS diagnostic status and mediates the relationship between psychological distress and symptom severity. Brain mechanisms underlying this relationship are unknown but may involve altered preparation for expected pain.

Their idea was simple, and the experiment--while weird--was well done and fairly straightforward. They set out with three hypotheses to test via fMRI; namely that patients with IBS would have:

(1) failure to inhibit arousal and limbic brain circuits during expectation, which would correlate with (2) affective stimulus ratings and (3) brain responses to the aversive stimulus.

What was so weird about this study was the way they induced expectation of pain:

The current study sought to characterize abnormalities in preparatory brain response before aversive pelvic visceral distention in irritable bowel syndrome (IBS) patients and their possible relationship to the consequences of distention.

(Emphasis mine.)

According to their visceral distention procedure:

Distention of the rectum was accomplished using a computer-driven pump (barostat) programmed to deliver phasic pressure steps (38 ml/s) separated by interinflation intervals at the resting pressure... All studies were performed after an 8 h fast and application of 2 Fleet enemas. Affective and perceptual responses to controlled rectal distention were assessed before the MRI protocol.

Basically they took a bunch of IBS patients and control subjects and inflated a balloon in their buttholes until it kinda hurt.

That must have been an interesting IRB meeting.

But you can't say that it's not an effective technique. How do you make people anxious about their bowels hurting? Well, you let them know you're about to make their bowels hurt by blowing up a balloon in their anus. QED.

So, what'd they find?

During anticipation of visceral pain, healthy subjects, but not IBS patients, downregulate homeostatic afferent processing network activity... Anticipatory downregulation is inhibited by negative emotions (stress, anxiety, anger), and these are higher in IBS patients.

The image above shows their major IBS patient finding.

Covariation of negative affect with anticipatory BOLD response. Higher BOLD signal during the cue period (less deactivation) was directly correlated with negative affect (p < 0.01; shown in red) in [the locus coeruleus] (location of crosshairs) and left amygdala (for anger and stress)...

There's a nice behavioral effect here, too, wherein:

Negative emotions support a competing strategy of tonic [locus coeruleus] arousal to disinhibit behavioral response, consistent with IBS patients having greater DBS and dACC activation during actual distention and false positive detection of interoceptive information (INS activity) during sham distention.

It's actually a really cool finding in a well-controlled study. It's just... kinda out there methodologically.

I'm not sure that I'd have volunteered as a control for that experiment.

Berman SM, Naliboff BD, Suyenobu B, Labus JS, Stains J, Ohning G, Kilpatrick L, Bueller JA, Ruby K, Jarcho J, & Mayer EA (2008). Reduced brainstem inhibition during anticipated pelvic visceral pain correlates with enhanced brain response to the visceral stimulus in women with irritable bowel syndrome. The Journal of neuroscience : the official journal of the Society for Neuroscience, 28 (2), 349-59 PMID: 18184777

On scientific outreach

2011-05-05T21:27:00.000-07:00

Neuroscience outreach has been an important part of my graduate career. I've talked about all of this stuff here before. This post isn't about me.

This post is, in a very small way, my attempt to thank the UC Berkeley Cognitive Science Student Association (CSSA).

Over the years I've done a lot of (often repetitive) talks for them, starting with the Feel Dead Brains lectures I inherited from a fellow neuroscience grad student, Aubrey Gilbert.

Every time I've done these talks the CSSA students have been super thankful and just outright awesome.

Although some researchers think that public lectures and outreach are pointless (or worse), I've found that public talks are a great way to meet some extremely smart, cool people.

And the CSSA has those in spades.

I've never met a more motivated group of undergraduate scientists. (Hell, I've rarely met career scientists as motivated as the CSSA members.) They're certainly a lot more engaged and organized than I was as an undergrad. They've run a conference for three years now, organized entirely by themselves, and attracted speakers such as John Searle, Patricia Churchland, Mike Merzenich, and George Lakoff.

It's great to see people so in love with the science, and I find that interacting with people at these kinds of public lectures helps reinvigorate my own interest. I hope that the CSSA students stay in touch through their own careers as they go on to become independent researchers.

Check out the video they made in preparation for this year's conference:

Thanks, CSSA.

TEDbrain

2011-04-28T16:11:00.000-07:00

TEDbrain: Dragging neuroscience into the 21^st century

(Source: Neil Girling)

That's me after my TEDxBerkeley last year. If I could do my talk again, it would be very different.

If it were tomorrow, I'd talk about how much more we could be doing in neuroscience if only some of the old walls were brought down. If only there was a way to bring together engineers, visual artists, designers, scientists, philosophers, mathematicians, etc. under one roof.

Not only do I want to see a TEDbrain, I want to see an entirely new research environment.

The mysteries of the brain aren't going to be solved with one, beautiful equation, or by a super-elegant experiment, or by a great new technique. The problem is bigger than that.

Understanding the brain isn't just a scientific problem, it's a data problem.

Granted there have been some amazing advances, but most cognitive neuroscience experiments are basically 1960s psychology experiments with better toys.

We can do better. We need to think bigger. We need to leverage the massive amounts of data we're collecting.

We need better data ontolgies. Better data mining. Better data visualization.

Right now, neuroscience in particular is undergoing a renaissance.

Hell, when you've got people like Sergey Brin who want to help spur on novel research, it strikes me as silly that a lot of the ways we're thinking about brain problems hasn't changed too drastically.

Neuroscience is fairly unique among the sciences in that it pulls in from so many different disciplines.

At Google last year, I gave a presentation titled, Computational Analysis Methods and Issues in Human Cognitive Neuroscience that was supposed to be about the difficulty we have in making the most out of the huge amounts of brain data that we collect from each of our subjects. We run very narrow experiments and throw out most of the information in our datasets by intentionally removing information via averaging, filtering, smoothing, a priori selection, etc.

Wasting data is stupid. But we all do it.

This winter, my wife and I put together brainSCANr in an attempt to synthesize and mine data from published research papers.

Tal Yarkoni and Russ Poldrack have done a more sophisticated job with PubBrain, which is a super cool, massive meta-analytic tool. Tal and Russ are doing an amazing job, but they're a rare breed.

My soon-to-be post-doc advisor, Adam Gazzaley, is doing awesome work in modernizing cognitive neurosciecne. At TEDxSanJose this year, he spoke about his work on taking neuroscience experiments out of the lab and into peoples' homes. About giving them at-home EEG and testing them using more natural stimuli (i.e., more "ethologically valid").

He and I have a really amazing project in the works.

The Bay Area is uniquely positioned at the interface of academic science and the intellectual tech communities. It would be the perfect place for a TEDbrain event.

The academic system around us is falling apart. Grant writing and politics make for a difficult environment for a researcher.

How is a scientist supposed to innovate when they're worried about their next grant? But I digress...

The 10 most cited neuroscience papers

2011-04-18T09:48:00.000-07:00

Over on Quora someone asked, "What are the most-cited works in neuroscience?"

As some of you may know, I love literature mining. I started brainSCANr with my wife to look at how neuroscience research is conducted. I've been talking with Neuroskeptic about looking at biases in how different neuroscience topics are studied.

This question on Quora piqued my interest, so I decided to try and work out the answer. I had to do some digging.

(source)

My first thought was of a retrospective published in Nature Reviews Neuroscience last year that revisited ten of its most-cited papers between 2000 and 2010: Ten years of Nature Reviews Neuroscience: insights from the highly cited.

A quick Google search showed that the Journal of Neuroscience also has a list of its most-cited papers on its site.

But in both of these cases we've got a clear bias: they only show the highly-cited articles published within their respective journals. And there are a lot of journals that publish neuroscience research.

Any answer I can find will come with a lot of caveats. It's difficult enough to define which papers are "neuroscience", let alone track down the "top cited" ones in an unbiased manner. From what I've seen, the most-cited papers tend to be methodological or crystallography structures. However, in order to reduce any sub-field bias, I wanted to find a database of papers to work from.

The ISI Web of Knowledge runs a site, ISI Highly Cited, wherein you can search by specific neuroscience researcher, but that information doesn't tell you about specific highly-cited papers. Cool, but no good here.

Thomson Reuters (who owns the Institute for Scientific Information (ISI)) also runs ProCite, which, thankfully, has a nice little site wherein they provide citation counts for 2610 neuroscience papers published in the ten-year period between 1995 and 2005. Those data come in a nicely-formatted text file.

Yay datas!

These types of files are data pornography for me. They make what I do so easy and fun!

(Yeah, I said it. Fun. What?)

(source)

Mind you, the results from ProCite come with caveats: I can't say that they're comprehensive (I don't know how they defined "neuroscience") and they're temporally restricted (1995-2005). Never the less, it's a good start.

Of those 2610 "highly cited" articles, 1877 had more than 100 citations. 1951 of the 2610 articles were classified as "research articles", 656 as "reviews" (and 3 as "notes"?) There were a total of 108 unique journals represented in this sample.

The breakdown by of the 20 journals with the largest number of highly-cited articles looks like this:

(Why yes, I do have a first-authored paper in three of those top five journals! I hadn't noticed! What? You'd like to give me a job? Why thank you! That would be delightful. ::COUGH::)

As an aside, I'd like to point out that 4 of the top 10 journals have one-word journal titles: Neuron, Nature, Science, and Neurology. Out of the 108 total journals represented, 22 have one-word titles. This means we should only see two--not four--one-word title journals in the top 10. This supports my pet theory that one-word title journals fare better than journals with longer titles. (This is a little ironic, because the journal with the longest title is also in the top 10: Proceedings of the National Academy of Sciences of the United States of America, but they've long since learned to refer to themselves simply as "PNAS".)

Of course, the earlier the year of the paper's publication, the more frequently it's been cited, which suggests that the citation counts for these articles will continue to increase (that is, after 10 years they still haven't really stopped getting cited).

Without further ado, here are the 10 most highly-cited neuroscience articles published between 1995 and 2005, ordered by number of citations:

1. (1684 citations) Sherrington et al., Cloning of a gene bearing missense mutations in early-onset familial Alzheimer's disease. Nature 1995.
2. (1603 citations) Polymeropoulos et al., Mutation in the alpha-synuclein gene identified in families with Parkinson's disease. Science 1997.
3. (1513 citations) Caterina et al., The capsaicin receptor: a heat-activated ion channel in the pain pathway. Nature 1997.
4. (1396 citations) Südhof, The synaptic vesicle cycle: a cascade of protein-protein interactions. Nature 1995.
5. (1369 citations) Pin & Duvoisin, The metabotropic glutamate receptors: structure and functions. Neuropharmacology 1995.
6. (1288 citations) Tessier-Lavigne & Goodman, The molecular biology of axon guidance. Science 1996.
7. (1246 citations) McKeith et al., Consensus guidelines for the clinical and pathologic diagnosis of dementia with Lewy bodies (DLB): report of the consortium on DLB international workshop. Neurology 1996.
8. (1186 citations) Games et al., Alzheimer-type neuropathology in transgenic mice overexpressing V717F beta-amyloid precursor protein. Nature 1995.
9. (1065 citations) Hsiao et al., Correlative memory deficits, Abeta elevation, and amyloid plaques in transgenic mice. Science 1996.
10. (1050 citations) Levy-Lahad et al., Candidate gene for the chromosome 1 familial Alzheimer's disease locus. Science 1995.

What's amazing to me is that 7 of the top ten papers are from Nature or Science, and 5 of them are more or less about Alzheimer's disease. This suggests a relative homogeneity of "top" researched topics.

As a final note, it's important to point out that these publications are from 1995-2005. They ignore older papers, as well as more recent ones. Given that the modern scientific publishing era began in 2003 with the founding of PloS and PLoS Biology, there wasn't really any time for papers published in those journals to really have any representation in this dataset.

Luo, L., Rodriguez, E., Jerbi, K., Lachaux, J., Martinerie, J., Corbetta, M., Shulman, G., Piomelli, D., Turrigiano, G., Nelson, S., Joëls, M., de Kloet, E., Holsboer, F., Amodio, D., Frith, C., Block, M., Zecca, L., Hong, J., Dantzer, R., Kelley, K., & (Bud) Craig, A. (2010). Ten years of Nature Reviews Neuroscience: insights from the highly cited Nature Reviews Neuroscience, 11 (10), 718-726 DOI: 10.1038/nrn2912
Sherrington R, Rogaev EI, Liang Y, Rogaeva EA, Levesque G, Ikeda M, Chi H, Lin C, Li G, Holman K, Tsuda T, Mar L, Foncin JF, Bruni AC, Montesi MP, Sorbi S, Rainero I, Pinessi L, Nee L, Chumakov I, Pollen D, Brookes A, Sanseau P, Polinsky RJ, Wasco W, Da Silva HA, Haines JL, Perkicak-Vance MA, Tanzi RE, Roses AD, Fraser PE, Rommens JM, & St George-Hyslop PH (1995). Cloning of a gene bearing missense mutations in early-onset familial Alzheimer's disease. Nature, 375 (6534), 754-60 PMID: 7596406
Polymeropoulos MH, Lavedan C, Leroy E, Ide SE, Dehejia A, Dutra A, Pike B, Root H, Rubenstein J, Boyer R, Stenroos ES, Chandrasekharappa S, Athanassiadou A, Papapetropoulos T, Johnson WG, Lazzarini AM, Duvoisin RC, Di Iorio G, Golbe LI, & Nussbaum RL (1997). Mutation in the alpha-synuclein gene identified in families with Parkinson's disease. Science (New York, N.Y.), 276 (5321), 2045-7 PMID: 9197268
Caterina MJ, Schumacher MA, Tominaga M, Rosen TA, Levine JD, & Julius D (1997). The capsaicin receptor: a heat-activated ion channel in the pain pathway. Nature, 389 (6653), 816-24 PMID: 9349813
Südhof TC (1995). The synaptic vesicle cycle: a cascade of protein-protein interactions. Nature, 375 (6533), 645-53 PMID: 7791897
Pin JP, & Duvoisin R (1995). The metabotropic glutamate receptors: structure and functions. Neuropharmacology, 34 (1), 1-26 PMID: 7623957
Tessier-Lavigne M, & Goodman CS (1996). The molecular biology of axon guidance. Science (New York, N.Y.), 274 (5290), 1123-33 PMID: 8895455
McKeith IG, Galasko D, Kosaka K, Perry EK, Dickson DW, Hansen LA, Salmon DP, Lowe J, Mirra SS, Byrne EJ, Lennox G, Quinn NP, Edwardson JA, Ince PG, Bergeron C, Burns A, Miller BL, Lovestone S, Collerton D, Jansen EN, Ballard C, de Vos RA, Wilcock GK, Jellinger KA, & Perry RH (1996). Consensus guidelines for the clinical and pathologic diagnosis of dementia with Lewy bodies (DLB): report of the consortium on DLB international workshop. Neurology, 47 (5), 1113-24 PMID: 8909416
Games D, Adams D, Alessandrini R, Barbour R, Berthelette P, Blackwell C, Carr T, Clemens J, Donaldson T, & Gillespie F (1995). Alzheimer-type neuropathology in transgenic mice overexpressing V717F beta-amyloid precursor protein. Nature, 373 (6514), 523-7 PMID: 7845465
Hsiao K, Chapman P, Nilsen S, Eckman C, Harigaya Y, Younkin S, Yang F, & Cole G (1996). Correlative memory deficits, Abeta elevation, and amyloid plaques in transgenic mice. Science (New York, N.Y.), 274 (5284), 99-102 PMID: 8810256
Levy-Lahad E, Wasco W, Poorkaj P, Romano DM, Oshima J, Pettingell WH, Yu CE, Jondro PD, Schmidt SD, & Wang K (1995). Candidate gene for the chromosome 1 familial Alzheimer's disease locus. Science (New York, N.Y.), 269 (5226), 973-7 PMID: 7638622

How to be an anti-scientist

2011-04-04T09:27:00.000-07:00

Along the lines of my "how to be a neuroscientist" post, I bring you: How to be an anti-scientist!

(Source - The Onion)

Example 1: Heliocentrism

Since [the astronomer] cannot in any way attain to the true causes, he will adopt whatever suppositions enable the motions to be computed correctly from the principles of geometry for the future as well as for the past... these hypotheses need not be true nor even probable.

Example 2: Evolution

This textbook contains material on evolution. Evolution is a theory, not a fact, regarding the origin of living things. This material should be approached with an open mind, studied carefully and critically considered.

The top quote is a preface to Copernicus's On the Revolutions secretly prepended without Copernicus's knowledge by a Christian theologian in the 1540s.

The bottom quote is a preface to biology textbooks distributed in Atlanta public high schools in 2002.

That gives us a Δt of approximately 460 years across which the complexity of the anti-science argument has gone from:

"...[T]hese hypotheses need not be true nor even probable."

to:

"[This scientific idea] is a theory, not a fact."

So, how does one succeed as an anti-scientist? Just keep repeating the same thing over and over again for centuries while the world around you changes ever faster.

More on oscillatory thoughts

2011-03-24T19:04:00.000-07:00

I've left a long and somewhat long-winded response to a question over on Quora, similar to my post last week on why we don't need a brain.

Are brain waves epiphenomena?
It is quite clear that by pooling the activity of many neurons or brain areas oscillations appear. But are the oscillations themselves causal? Do my fellow quora users know of any particular authors or references that present skeptical accounts on the causal role of oscillations?

I've touched on this topic several times here before (it is my blog's namesake, after all), but I figured I'd go over it again here.

Anyway, this response also acts as a response to a question I got on Twitter when I put out a call for neuroscience questions.

@roteno asked:

I'd be interested in knowing more. Perhaps a "Brain Signaling for Dummies (with EE degrees & EMF backgrounds)"

I count my Quora response as a good enough response to that one, too :)