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21.7.11

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

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.

13.7.11

Why Netflixs' price hike is a brilliant move

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.

12.7.11

Working memory and cognitive enhancement

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. ResearchBlogging.org 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

6.7.11

The top 11 (or 23) unanswered questions in neuroscience

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 Reply



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 Reply



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.

ResearchBlogging.org
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