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Archive for the ‘modularity’ Category

Recently, a team in Cambridge has developed a diagnostic tool for prosopagnosia, a rare disorder of face perception where the ability to recognize faces is impaired, although the ability to recognize objects may be relatively intact. While this work has made it easier to sort out between those who are truly prosopagnosic and those who have a more global agnosia, a recent report shows that prosopagnosia is much more common that you would think.

An impressive 2 percent of the population may have some fom of prosopagnosia! That means that millions of people are not only poor but disastrous at recognizing faces, even from famous people.

You can read more about the story at ScienceDaily, visit the faceblind.org website, or read the papers yourself from Ken Nakayama's homepage

So next time you meet a person whos name you've forgotten, don't worry. At least you're not prosopagnosic!

-Thomas 

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In a thorough and very good review in PLoS Genetics, James Sikela writes about the comparative genetics between the chimp and the human genome. From the article:

It has been pointed out that the primary molecular mechanisms underlying genome evolution are 1) single nucleotide polymorphisms, 2) gene/segmental duplications, and 3) genome rearrangement. In addition, a “less-is-more” hypothesis has been proposed that argues loss of genetic material may also be a source of evolutionary change. Given these factors, what are we learning about their respective roles now that we can compare multiple primate genome sequences?

As we have pointed out repeatedly in this blog, the study of genetic influence on the brain is going to change our understanding of what a human is, how and why our thoughts are formed (and restricted) the way they are. This review surely puts the finger on the pulse and notes:

One of the most important findings to emerge from the latest human and primate genome-wide studies is that a fundamental assumption underlying this model has changed: the interspecies genomic changes are numerous and diverse, and, as a result, there appear to be many additional types of genomic mechanisms and features that could also be important to the evolution of lineage-specific traits. Given this new perspective, we now know that the degree of difference between our genome and that of the chimp depends on where, and how comprehensively, we look. The multitude of genomic differences that we now know exists should provide an abundance of fertile genomic ground from which important lineage-specific phenotypes, such as enhanced cognition, could have emerged. 

Here is the abstract:

The jewels of our genome: the search for the genomic changes underlying the evolutionary unique capacities of the human brain

James M. Sikela

The recent publication of the initial sequence and analysis of the chimp genome allows us, for the first time, to compare our genome with that of our closest living evolutionary relative. With more primate genome sequences being pursued, and with other genome-wide, cross-species comparative techniques emerging, we are entering an era in which we will be able to carry out genomic comparisons of unprecedented scope and detail. These studies should yield a bounty of new insights about the genes and genomic features that are unique to our species as well as those that are unique to other primate lineages, and may begin to causally link some of these to lineage-specific phenotypic characteristics. The most intriguing potential of these new approaches will be in the area of evolutionary neurogenomics and in the possibility that the key human lineage–specific (HLS) genomic changes that underlie the evolution of the human brain will be identified. Such new knowledge should provide fresh insights into neuronal development and higher cognitive function and dysfunction, and may possibly uncover biological mechanisms for information storage, analysis, and retrieval never previously seen.

-Thomas 

______________________________

John Hawks has a very good discussion about this article. 

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(This is a follow-up on Martins and my brief review)

In the latest issue of Trends in Cognitive Sciences, Kovas and Plomin has an article about the implications of "generalist genes", should the theory be correct. The "generalist genes hypothesis" states that the same genes affect most cognitive abilities and disabilities. That is, our diverse cognitive apparatus — from language, to working memory, to visual attention — is affected by a few genes alone. This thought runs straight counter to the idea that genes can be responsible for one cognitive function alone.

Kovas and Plomin speculate about the meaning of generalist genes for our theories of how the brain works. From the article:

One possibility is that a generalist gene affects a single brain area or function that in turn influences several cognitive processes. The effect of such a gene would be general at the cognitive level, but specific at the level of localization in the brain. In other words, the structures and functions of the brain are uncorrelated genetically because they are influenced by different genes. We consider that this possibility is unlikely because pleiotropy suggests that any gene is likely to be expressed in more than one structure or function.

A second possibility is that cognition-related generalist genes pleiotropically affect multiple brain structures and functions, but each of these structures and functions affects a specific cognitive process. In other words, the structure and function of these specialized areas are correlated genetically because the same genetic polymorphism affects these different regions. Even though each brain structure and function is associated with one specific cognitive process, these cognitive processes are correlated genetically because the brain processes are correlated genetically.

The most likely possibility in our opinion is that generalist genes affect multiple brain structures and functions, each of which affects multiple cognitive processes. This mechanism would lead to genetic correlations both in the brain and in the mind.

I assume that generalist genes is initially incompatible with the thought of massive modularity as we see in evolutionary psychology. That does not rule out, however, the possibility of incorporating generalist gene'ism with EP. Yes, we can say that cognitive functions have evolved separately, but they might still be built out of the same genetic foundation. No need for logical inconsistency, as far as I can see.

-Thomas 

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As the community — and thought — about imaging genetics grows, new studies are emerging. These studies focus on the way that genes are found to play a role in different cognitive functions. In a recent special issue of Behavior Genetics, the focus is on the progress in the linkage between the genetic map and behavioural traits. There are a lot of interesting articles in this special issue, altough I find a few especially intriguing.

In a nice review, Steven Buyske reviews different findings that map cognitive functions and the gene map. Here's the abstract:

Cognitive Traits Link to Human Chromosomal Regions

Human cognition in normal and disease states is both environmentally and genetically mediated. Except for measures of language-specific abilities, however, few cognitive measures have been associated with specific genes or chromosomal regions. We performed genome-wide linkage analysis of five neuropsychological tests in the Collaborative Study on Genetics of Alcoholism sample. The sample included 1579 individuals (53% female, 76% White Non-Hispanic) in 217 families. There were 390 markers with mean intermarker distance of 9.6 cM. Performance on the Digit Symbol Substitution Test, a component of the Wechsler Adult Intelligence Scale-R, showed significant linkage to 14q11.2 and suggestive linkage to 14q24.2. This test of sustained visual attention also involves visual-motor coordination and executive functions. Performance on the WAIS-R Digit Span Test of immediate memory and mental flexibility showed suggestive linkage to 11q25. Although the validity of these results beyond populations with a susceptibility for alcohol dependence is unclear, these results are among the first linkage results for non-language components of cognition.

But hey, there's more. There are studies on the association of genes and anxiety and neuroticism; gene association of feelings of loneliness; gene association to age at first cigarette; genes on academic skills; and genes on IQ (of course).

The question is: where will it end? Of course, genes are abundantly represented in the body. They are, after all, the receipt to every cell and how they should work. But what level of description and explanation should we apply in this gene-to-cognition mapping? I fear that at least in some studies, old "folk-psychological" concepts about cognitive traits are compared to high-detailed analysis and knowledge about the genes. In order to understand how genes get expressed in a way that they shape behaviour, we need to work out the intermediate stages. We need to know how genes influence neurons, transmitters, plasticity on one level; how they shape interacting neurons and neural assemblies; and finally how this cumulates into one or the other kinds of behaviour. The leap from gene to behaviour is, IMHO, too wide. The solution is in the nitty-gritty details.

Way to go CIMBI!

-Thomas

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Here's another new feature here at BrainEthics. Some quotes from neuroscience and related fields are so provocatively refreshing that they deserve a place of their own. Why not highlight them here, as we fall upon them. Quotes are great, since they seem to grasp the ghist of a whole idea, in one or a few sentences it captures the meaning of an entire book, a whole research trend, a misconjecture in the literature.

I'll start off with this great quote from Gilles Laurent, who writes in a chapter in a recently published, interesting book (worth mentioning in a post of its own) called "23 problems in system neuroscience". Here, Laurent opposes what he sees as a cortico-centrism; an unwarranted fascination with the cerebral cortex at the expense of subcortical (and other) structures:

"Why this obsession with cortex? (…) most scientists act as if King Cortex appeared one bright morning out of nowhere, leaving in the mud a zoo of robotic critters, prisoners of their flawed designs and obviously incapable of perception, feeling, pain, sleep, or emotions, to name but a few of their deficiencies. How nineteenth century!"

-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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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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