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Archive for April, 2006

Ever heard about evidence-based medicine? Now we should all start talking about evidence-based teaching (or paedagogics), too. Usha Goswami has a nice article in Nature Reviews Neuroscience about the way that (neuro-)science should be communicated to teachers, who again should implement these ideas in schools. I'm all in for it, although I think we should be careful about saying too much and feel too confident that our word may come through the way we want it to. there are a lot of flaky uses of science terms in software, teaching applications and so forth, to feel confident that we may do well enough to bring the correct information to the fore. As Goswami also writes in his paper, much of the current science-based talks are "reality testers" that ultimately point out how that other approaches are plain wrong. This may very well backfire. As he writes:

(…) At the Cambridge conference, prominent neuroscientists working in areas such as literacy, numeracy, IQ, learning, social cognition and ADHD spoke directly to teachers about the scientific evidence being gathered in scientists' laboratories. The teachers were amazed by how little was known. Although there was enthusiasm for and appreciation of getting first-hand information, this was coupled with frustration at hearing that many of the brain-based programmes currently in schools had no scientific basis. The frustration arose because the neuroscientists were not telling the teachers 'what works instead'. One delegate said that the conference "Left teachers feeling [that] they had lots stripped away from them and nothing put in [its] place". Another commented that "Class teachers will take on new initiatives if they are sold on the benefits for the children. Ultimately this is where brains live!".

-Thomas

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What happens to the brain as we age? Today, we know that the brain as a whole becomes smaller, it atrophies. As the brain develops, we know from studies like the ones performed by Sowell et al. that regions such as the primary sensory and motor areas mature early in the lifespan, while areas such as the prefrontal cortex mature very late.

Now, tying the evidence from development and ageing together, we can see how the brain changes over the lifespan. This is, of course, only partly true. We can study people at different ages at one time to get an estimate of how large brains and regions are in age-, gender- and educationally comparable groups people. Such cohort studies have the drawback that they do not tell us anything about how the individual brain changes over time. For that we have longitudinal studies. These studies very clearly shows how the brain changes over a few years. Together, these studies show much the same picture: brain changes dramatically as we age. We can put this into a few points:

Neural ageing is region specific: If we look at different area of the brain, we can see that the regions differ in how they age. Some structures mature early and degenerate late. Others mature late and degenerate early.

Neural ageing is non-linear: Previous models of ageing used linear models to understand the changes occuring in the brain over age spans. More recent studies now demonstrate that non-linear models fit better to the data.

These points can be seen in the following images. They show the size of the hippocampus (top) and nucleus accumbens (bottom). This is to demonstrate three points: 1) that the changes according to age are non-linear; 2) that the changes are region specific, and; 3) that there is a great variability in the relative size of each structure.

Hippocampus ageing Nucleus Accumbens

Now to my main point. Can we assume that the individual differences are "stable", in the way that people with larger-than-mean hippocampi will always stay larger than the mean? Or is the opposite true; that there are very individual trajectories in how the brain develops and ages? IMO, whether one model is true and than other false has potential high impact on our treatment in different settings. This problem is illustrated by a figure by Terry Jernigan at our lab that I reproduce here. The example shows age changes in dorsolateral prefrontal cortex. The mean is shown as the green line. The other lines indicate hypothetical trajectories for individuals. In other words, the PfC may change in a very individual manner.

Age-related volume changes in the dlPfC

Think, for example, about teaching in schools. In a country such as Denmark, teaching is rather homogenous, the same curriculum is applied in every school, the same tests etc. And your belonging to one particular class is defined by your chronological age. As I see it, this is based on the assumption that our mental capacities follow the same trajectory: those with a good learning ability will always stay high, those who are low will stay low. As a mean approach, we use age as the least common demoninator to define your group belonging.

So the question arises here: what if it turns out that development (and ageing in general) is very individual, non-linear and not stable relative to the mean? What if a person with a large prefrontal cortex at age 8 will have a below mean size at age 14, and then end up by a larger structure at 25? Would this make it harder or easier to do teaching, training or other interventions with people? Does it mean that we should re-consider our (Danish/Scandinavian) ways of teaching and assigning kids into age-dependent classes? I'm just asking. Feel free to comment.

-Thomas

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Nikos LogothetisYesterday, Nikos Logothetis gave a great talk at the annual keynote lecture for the Copenhagen University Research Priority Area "Body and Mind". In the lecture, Logothetis touched upon several issues on the workings of the brain – from his perspective. But at the later Master-class where it was possible to have a one-to-one discussion with him, there was little doubt about Logothetis' view about how to understand the workings of the brain and mind. And especially how to study it with neuroimaging techniques.

BOLD fMRI, he claims, can tell us something about where in the brain something is happening. But other than that, it can tell us very little about what happens in that region. In other words, Logothetis is not fascinated by the current "blobology" (AKA neo-phrenology) that is seen in much of today's neuroimaging research papers. Logothetis argues that in order to say anything intelligible about brain function, we need to go beyond the current focus on where in the brain something is happening. We need to move towards integrating multiple imaging modalities in order to get a better picture of neural processes. Logothetis himself suggested and talked mostly about EEG and deep electrodes, and MEG, in combination with BOLD fMRI. But at the master class Logothetis also discussed the use of multiple MRI modalities such as the combination of perfusion MRI (Arterial Spin Labeing) and BOLD fMRI. But BOLD alone? No way!Multimodal approach to imaging ageing

To the right you can see the key slide from my talk at the Master class, positing the problem of combining measurements of perfusion and atrophy to BOLD fMRI measures, as co-variates. In ageing studies, we can see BOLD fMRI changes, but there is a question whether the well-known changes in brain perfusion and atrophy plays a role in chaning the BOLD signal. That was my question to Logothetis. Click on the image to see the full details.

Oh, and did I mention that Logothetis gives little for the current neo-phrenological thoughts about a 1:1 match between a cognitive function and a brain area? The brain doesn't work that way…

-Thomas

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_blogmondaymorning.jpgAnother Monday, another round of interesting papers from the world of neuroscience.

Today, I only have a few, but all are worth checking out!

In relation to my post yesterday about the evolutionary origins of language I want to direct your attention to another interesting paper forthcoming in Brain and Language. Its topic is pretty well captured by the authors' – Francisco Aboitiz and Ricardo R. Garcia – abstract: "In this paper, we suggest that other linguistic phenomena like semantic and syntactic processing also rely on the activation of transient memory networks, which can be compared to active memory networks in the primate. Consequently, short-term cortical memory ensembles that participate in language processing can be phylogenetically tracked to more simple networks present in the primate brain, which became increasingly complex in hominid evolution. This perspective is discussed in the context of two current interpretations of language origins, the “mirror-system hypothesis” and generativist grammar." [Link to paper.]

As we all know, obesity is a growing health problem in the Western world. Its cause is pretty straightforward: We eat more than we need. But why? The key to that answer lies in the brain's reward system and how it works to promote food intake through the feeling of hedonic pleasure. In the next issue of Brain Research Reviews Daniela Cota and her colleagues have a great review of what is today known about this hugely important system. [Link to paper.]

Deductive reasoning is probably a unique human ability, so of course there is a natural interest in understanding the neuronal processes underlying this special form of reasoning. In the March issue of Journal of Cognitive Neuroscience Thomas Fangmeier and colleagues present evidence for a three-stae model of deductive reasoning. They write: "We specifically focused on three temporally separable phases: (1) the premise processing phase, (2) the premise integration phase, and (3) the validation phase in which reasoners decide whether a conclusion logically follows from the premises. We found distinct patterns of cortical activity during these phases, with initial temporooccipital activation shifting to the prefrontal cortex and then to the parietal cortex during the reasoning process. Activity in these latter regions was specific to reasoning, as it was significantly decreased during matched working memory problems with identical premises and equal working memory load." [Link to paper.]

More highlights from the literature next Monday!

– Martin

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Let me point you to a nice article, by Simon Fisher and Gary Marcus, in the January issue of Nature Reviews Genetics. Fisher was one of the co-discovers of the link between a verbal dyspraxia disorder in an English family and a point mutation on the FOXP2 gene. Marcus, a former student of Steven Pinker, is well-known for his critique of connectionist models of language-aquisition. Although I personally think it overstates the case for innate modules, I wholeheartedly recommend Marcus' book The Birth of the Mind which is, as far as I know, the first, and still only, popular account of what is known today about the genetic basis of brain development. Together, they have earlier written a review of the FOXP2 story in Trends in Cognitive Science. The present paper aims to show how genetical studies can aid our understading of the evolution of language.

In recent years interest in this topic has been booming. A large number of possible adaptative causes have been proposed by a range of researchers. [Language Evolution, edited by Morten Christiansen and Simon Kirby, will give you a short overview of most of these hypotheses.] There is a problem with this approach, though, in that it tends to focus on just one magical change in hominid behaviour, with the accompaying change to the brain being passed on to following generations. To take one prominent example, Robin Dunbar, for instance, sees the decisive moment in the evolution of language to be the expansion of hominid social groups, some time around the appearance of homo erectus, making it advantageous to be able to keep account of the larger number of conspecifics through communication. Dunbar speculates that a change in our ability to mentalize – sometimes also referred to as Theory of Mind – could be the new cognitive function to have facilitated this improved capacity for social communication. Another, more simpleminded hypothesis, is the still widespread idea that neuronal changes to Broca's area brought about a novel ability to string together words into syntactical phrases.

But, as more and more becomes known about the brain processes underlying language, it appears increasingly unrealistic that any such single-stroke wave of the magic wand will suffice to explain the emergence of language. The neural language system is enormously complex and encompasses, to just name a few things, auditory analysis, conceptual knowledge and memory, semantic selection processes, motor control, and a great number of other functions. It stands to reason that all these processes must have evolved on an individual basis. It is therefore much more probable that the evolution of language has gone through several different adaptive events since the last common forefather of homo and pan.

This is exactly the approach taken by Fisher and Marcus. They call it "descent with modification", and write that "[in this paper] we argue that language should be viewed not as a wholesale innovation, but as a complex reconfiguration of ancestral system that have been adapted in evolutionarily novel ways". The offshot of this approach is that the evolution of language can be studied by comparing human genetics and neurobiology to other species. Write Fisher and Marcus:

(…) although non-human primate communication shows qualitative differences from human language, studies have established that most components of language how some degree of continuity with other species. For example, the human vocal tract supports a wider epertoire of speech sounds than could be produced by other primates, but the capacity to create richly modulated formants is not unique to humans. Likewise, many animals and birds can distinguish different human speech sounds, and adult tamarin monkeys can discriminate between the distinctive rhythmic properties of different languages. Debate continues about exactly how much of the machinery of language is species – or language – specific; for example, opinion is divided over whether recursion represents the only component that is genuinely new to the human species. Nevertheless, views that consider language to be fully independent of ancestral systems are no longer tenable, and there is a growing recognition that cognitive, physiological, neuroanatomical and genetic data from non-speaking species can greatly inform our understanding of the nature and evolution of language.

The bulk of Fisher and Marcus' paper is dedicated to a review of methods for such genetical comparisons of humans to other species. But its true importance lies in the way it dismantles the adaptionist programme in evolutionary psychology. Like language, social cognition, reasoning, and other forms of cognition, are in most cases complex amalgams of a range of neurobiological processes, and therefore very unlikely the product of "wholesale innovation". A more precise picture of the evolution of human cognition is to be found through an detailed understanding of how the human brain differs from other species, and through a comparison of the genes and gene-expression systems characterising these species.
Reference

Fiser, S. & Marcus, G. (2006): The eloquent ape: genes, brains and the evolution of language. Nature Reviews Genetics 7: 9-20. [The paper can be downloaded from Marcus's homepage.]

-Martin

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The visual word form area (VWFA) is one of the most contested concepts of modern neuroscience. Its proponents claim that a dedicated slice of cortex in the occipitotemporal region of the brain – probably centered on the fusiform gyrus – underlie the ability to read. The most radical version of this hypothesis states that the VWFA is a specialized module – an idea that implicates some sort of genetical determinism. Since writing only has been around for some 6000 years many researchers doubt that there have been enough time for such a module to evolve. Instead, they expect reading to piggybackride on other, perhaps more general, visual processes.

The April 20 issue of Neuron contains a case study of man surgically treated for epilepsy that bears on these questions. As a consequence of excision of cortical tissue posterior to the putative VWFA this patient developed a case of pure alexia where, whereas before surgery he took ~600 ms to read a word, regardless of word lenght, after surgery his reading slowed to ~1000 ms for three-letter words and increased by ~100 ms per additional letter.

Crucially, postsurgical fMRI tests showed that the VWFA no longer responded more to words than to other objects, even when words were contrasted with viewing a simple fixation point. The authors suggest that this lack of activation is explained by the fact that postsurgically the VWFA is no longer receiving its normal input. Instead, a more widespread activation pattern, including frontal, parietal, and temporal sites, appear to "take over", resulting in a letter-by-letter reading strategy.

While the study clearly demonstrates that the VWFA plays some kind of (important) role in reading, it doesn't really illuminate what type of function the VWFA performs. And, at the same time, it cannot be said to settle the question of modularity, since the patient was a 46-old man who, of course, has had amble time to develop a reading skill from learning. As Alex Martin notes in a great accompanying resumé, the study do, however, leaves unresolved "the vexing problem of how to account for the intersubject consistency in the general location of the VWFA and other category-related regions in ventral occipitotemporal cortex. One possibility is that the VWFA performs a visual processing function that predisposed it to being co-opted for reading." But there may also be other reasons. In any case, it is a very nice study that will prove important for further debates on both reading and modularity.

Reference

Gaillard, R. et al. (2006): Direct intracranial, fMRI, and lesion evidence for the causal role of left inferotemporal cortex in reding. Neuron 50: 191-204.

Martin, A. (2006): Shades of Déjerine – forging a causal link between the visual word form area and reading. Neuron 50: 173-175.

-Martin

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Update. If you haven't already noticed it, yesterday a reader posted a reply by Henry Stapp to Christof Koch's recent Nature article in the comments-section to my post on Koch's paper. I don't know if it is Dr Stapp himself who has graced our blog with a visit, but you should take the time to read through his rebuttal of Koch's arguments!

– Martin

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