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Archive for June, 2006

Genetics is increasingly making itself felt in the word of neuroscience. Labs all over the world are trying to understand the role played the the genome in the development of the brain, and impressive results are published each month highlighting how genes are expressed in the working brain, influencing learning and behaviour.

The holy grail of this neurogenomic research is, of course, the establishment of a bridge between the genome, the cell biology of neurons and synapses, the neurobiology of cognitive mechanisms, and behaviour – i.e., the four major aspects of the human mind. So far, not many behavioural traits – if any – can be explained fully in terms of the neurobiological mechanisms causing it, the molecular processes involved in said mechanisms, and the genomics underlying it all, but tintalizing results are emerging all the time that hint at what will come. The Hariri experiments Thomas and I have posted about here on the blog constitute one example. The tracing of how gene expression correlates with the learning of songs in song birds is another. [Check out these two sites.]

In lieu of all this, Cognition has decided to put together a special issue reviewing the progress made in genetics relating to the understanding of human cognition. The issue is still in press, but it is already possible to read some of the papers on the journal's webpage. As far as I can tell from the editorial introduction, written by Franck Ramus [available here], the special issue will contain contributions by Simon Fisher, Evan Balaban, Karin Stromswold, Bruce Pennington, James Blair, and Gary Marcus. Of these, Fisher's paper ["Tangled webs: Tracing the connections between genes and cognition"], Balaban's ["Cognitive developmental biology: History, process and fortune's wheel"], and Marcus' ["Cognitive architecture and descent with modification"] are on-line as I write this. I have glanced quickly at the available articles, and from what I can gather they look especially relevant to researchers working within the cognitive neurosciences who are interested in knowing more about how neurogenomics will impact their work.

Naturally, any attempts to root cognition in genetics will stir up controversies, and raise numerous hard questions. I will return to some of these issues in the coming weeks, as I read my way through the paper. Teaser: You are definitly going to hear more about modularity in the coming days!

-Martin

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Monday Paper Survey, June 12

I missed the paper survey last week, but this week we are back in full effect (albeit a day late!).

English,German and Japanese language researchers led by Cathy Price demonstrates in a fMRI study published in Friday's Science that the left caudate nucleus plays an important role in monitoring and controlling which language is used by bilinguals. German-English and Japanese-English bilinguals were tested on a semantic task, and neuronal responses within the left caudate turned out to be sensitive to changes in the language used or the meaning of the words read by the subjects. Very interesting! Incidentaly, voxel-based morphometry analysis of the affected members of the KE Family (where a point mutation on the FOXP2 gene has led to aphasia) showed abnormalities in the caudate nucleus. So, perhaps the time has come for a more concerted investigation into the role played by the caudate in language production and comprehension. [Link to paper.]

Oxford University Press is starting a new journal this summer called Social Cognitive and Affective Neuroscience. Mattew Lieberman is the editor. If you have an institutional access to OUP's journals, you can find a number of paper in press here. Ray Dolan, Hugo Critchley and their group at FIL in London report an intersting experiment targeting the neuronal mechanisms engaged in the processing of sadness. From the paper's abstract: "We investigated whether observed pupil size modulates our perception of other’s emotional expressions and examined the central mechanisms modulated by incidental perception of pupil size in emotional facial expressions. We show that diminishing pupil size enhances ratings of emotional intensity and valence for sad, but not happy, angry or neutral facial expressions. This effect was associated with modulation of neural activity within cortical and subcortical regions implicated in social cognition. In an identical context, we show that the observed pupil size was mirrored by the observers’ own pupil size. This empathetic contagion engaged the brainstem papillary control nuclei (Edinger–Westphal) in proportion to individual subject’s sensitivity to this effect. These findings provide evidence that perception–action mechanisms extend to non-volitional operations of the autonomic nervous system." [Link to paper.] Another fascinating study by Marco Iacobini's group demonstrate that repetitive TMS stimulation of the right parietal cortex induces a "virtual lesion" that disrupts the ability to discriminate between your ow face and that of others. Wow! [Link to paper.]

 

The hyperscanning guys from Baylor College of Medicine in Houston and CalTech have a new paper out concerning the neurobiology of social exchange (Science, May 19, 2006). From the abstract: "During a social exchange with a partner, one fundamental variable that must be computed correctly is who gets credit for a shared outcome; this assignment is crucial for deciding on an optimal level of cooperation that avoids simple exploitation. We carried out an iterated, two-person economic exchange and made simultaneous hemodynamic measurements from each player’s brain. These joint measurements revealed agent-specific responses in the social domain (‘‘me’’ and ‘‘not me’’) arranged in a systematic spatial pattern along the cingulate cortex. This systematic response pattern did not depend on metrical aspects of the exchange, and it disappeared completely in the absence of a responding partner." [Link to paper.] Now, just what is the cingulum doing!

-Martin

 

 

 

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Volume 13, issue 5 of the Journal of Clinical Neuroscience contains – in my opinion – a very strange article. It's called "Ethics in medical technologies: The Roman Catholic viewpoint" and is written by Joseph Życiński. I found a wiki-like version of the paper here. The article is not strange because of its topic per se, which is bioethics from a religious point of view. What I find strange is that the article is published in a peer-reviewed scientific journal, and worse, that it is filled with religious dogma that are presented as axiomatic truths. 

Even accepting these strange facts, I find it unacceptable that the article does not discuss critically other approaches such as Gazzaniga's recent book "The ethical brain" (see my blog entry here). With statements such as

According to Christian ethics, we are called upon to treat each and every living member of the human species, including the embryo, as a human person with fundamental rights, the first of which is the right to life.

… I wonder if the insightful criticism of Gazzaniga has ever been read or heard by Życiński. In this way, we can only guess at what the author's opinion is on more scientifically informed viewpoints.

Here is the abstract:

Ethics in medical technologies: The Roman Catholic viewpoint.

Zyciński J

J Clin Neurosci. 2006 May 4;

New medical techniques and novel scientific discoveries bring many basic questions concerning the role of human dignity in medical research as well as in the society of the future. This paper presents the Roman Catholic approach to the use of new technologies, the research of human embryos, the ethical aspects of studies on the human genome. The concept of "human ecology", as proposed by John Paul II, is introduced to reconcile the academic freedom of research with insurmountable ethical barriers which must be recognized to defend human dignity. In critical appraisal of Peter Singer's concept of the quality of life the author points out that it is irrational to try to reduce this quality to the level of biological parameters. Human dignity as well as the sanctity of life express also a quality of life so important for the cultural growth of Homo sapiens. To protect human ecology it is our moral duty to defend human dignity and to recognize the importance of those values that are fundamental in the process of development of the human species.

And speaking of Gazzaniga, I should definitely remember to write the following parts of the book presentation.

-Thomas 

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We've just received an interesting report written by Bärbel Hüsing, Lutz Jäncke and Brigitte Tag assessing the impact of the various neuroimaging tools available today. It attempts to survey how these brain imaging techniques are used, both in clinical and in cognitive neuroscience. It discusses the costs associated with the individual imaging techniques, the training requirements of the researchers conducting imaging experiments, and the safety of patients and subjects. Interestingly, it also dives into many of neuroethical questions discussed here on BrainEthics, including the use of neuroimaging to inform pedagogy, marketing, and "forensic psychology" (read: lie detection). In short, it will interest all people mindful of the neuroethical consequences of neuroimaging research.

I've just started reading the book. When finished I will post a more detailed review here on the blog.

 

 

-Martin

Reference

B. Hüsing, L. Jäncke & B. Tag (2006): Impact Assessment of Neuroimaging. Zürich: IOS Press. [Link to publisher's site.]

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As we age, genes are expressed differently throughout our body. The most obvious examples are the hormonal changes seen in adolescence and in the menopause. In many models of how genes are expressed during older age, one of the prevalent models – the programmed ageing model – claims that ageing is caused by genetically programmed cell death. In other words, ageing is programmed into our cells – little blame is normally to be put on random or environmental factors.

Opposed to this model we have the normally less favoured stochastic model, which claims that random biological events play a significant role in ageing. In a recent report (PDF) (see also more extensive material here (PDF)) in Current Biology a team of researchers from the Max Planck Institute for Evolutionary Anthropology, headed by Mehmet Somel, present evidence supporting this model. Using an in-house method (called "age-correlated heterogeneity of expression", or ACHE) to assess heterogeneity of gene expression, they found that the expression becomes more heterogeneous as we age. And this goes not only for humans. Rats show the same pattern, too. They find that their results "are compatible with ACHE being an outcome of the accumulation of stochastic effects at the cellular level". In other words, something that is not programmed but due to other biological factors.

You can see this in the following figure from the article:

heterogeneity.jpg

Explanation: "An example from the human brain data set B, the log-expression versus age plot for a probe set detecting the gene PIM-1, for which the ACHE test p-value was calculated as0.0002."
Looks like heterogeneity to me … although I'd like to see some more data, maybe on 100-200 subjects.

Note also from that article that the heterogeneity is different depending on where in the body we take the sample. What I find interesting is that the brain seems to be one of the organs where genes become most heterogeneous during ageing (see bar 2-5). This also goes for the rat hippocampus. Click the image to see a larger version:
heterogeneity2.jpg

Explanation: The heights of the bars indicate observed to expected ratios of the number of probe sets at different cutoffs within the ACHE test p-value distribution

But what is ACHE really a measure of? Here's the answer from Somel et al.:

Our results indicate that ACHE is a general — but weak — effect in the transcriptome.This is compatible with ACHE being the outcome of accumulating stochastic effects in the soma, such as cellular damage and mutations. These effects will influence each cell in a unique way so that expression variation among aging cells will be equalized at the tissue level. If somatic mutations mostly cause decreases in expression level, the overlap between ACHE and age- related decrease in expression levels can also be explained within this framework. ACHE supports the stochastic nature attributed to the aging process. It implies a weakening of expression regulation with age, contrary to previous observations and hypotheses based on measurements on a small number of gene.

While browsing around for links to this post, I found a great forthcoming publication (PDF) in Trends in Ecology and Evolution by Partridge and Gems. See also this nice yet brief post at Wikipedia about the ageing brain.

-Thomas

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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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Today's featured article at Wikipedia is about transhumanism, "an international intellectual and cultural movement supporting the use of new sciences and technologies to enhance human physical and cognitiveameliorate what it regards as harsh and unnecessary aspects of the human condition, such as disease and aging." If you think of humanism as the attempt to help every person reach her or his full potential (whatever that means; as if we have an inborn potential), transhumanism goes beyond this and asks whether we can go beyond the "naturally given" potential and expand our possibilities — and reach them.

Some, however, mean that transhumanism is one of "the greatest threat to the welfare of humanity" today, as suggested by Francis Fukuyama. The basic idea in Fukuyama's criticism is that Transhumanism leads to inequality between humans:

Underlying this idea of the equality of rights is the belief that we all possess a human essence that dwarfs manifest differences in skin color, beauty, and even intelligence. This essence, and the view that individuals therefore have inherent value, is at the heart of political liberalism. But modifying that essence is the core of the transhumanist project. If we start transforming ourselves into something superior, what rights will these enhanced creatures claim, and what rights will they possess when compared to those left behind? If some move ahead, can anyone afford not to follow? These questions are troubling enough within rich, developed societies. Add in the implications for citizens of the worlds poorest countriesfor whom biotechnologys marvels likely will be out of reachand the threat to the idea of equality becomes even more menacing.

Transhumanisms advocates think they understand what constitutes a good human being, and they are happy to leave behind the limited, mortal, natural beings they see around them in favor of something better. But do they really comprehend ultimate human goods? (…)

A response by Nick Boström can be found here. He criticizes Fukuyama on three points:

  1. The assumption that there is a unique “human essence”
  2. Only those individuals who have this mysterious essence can have intrinsic value and deserve equal rights
  3. The enhancements that transhumanists advocate would eliminate this essence. From this, he infers that the transhumanist project would destroy the basis of equal rights.

Against the idea of "human essence", Boström argues:

The concept of such a “human essence” is, of course, deeply problematic. Evolutionary biologists note that the human gene pool is in constant flux and talk of our genes as giving rise to an “extended phenotype” that includes not only our bodies but also our artifacts and institutions. Ethologists have over the past couple of decades revealed just how similar we are to our great primate relatives. A thick concept of human essence has arguably become an anachronism.

(…)

The only defensible way of basing moral status on human essence is by giving “essence” a very broad definition; say as “possessing the capacity for moral agency”. But if we use such an interpretation, then Fukuyama’s third premise fails. The enhancements that transhumanists advocate – longer healthy lifespan, better memory, more control over emotions, etc. – would not deprive people of the capacity for moral agency. If anything, these enhancements would safeguard and expand the reach of moral agency.

Boström concludes:

Fukuyama’s argument against transhumanism is flawed. Nevertheless, he is right to draw attention to the social and political implications of the increasing use of technology to transform human capacities. We will indeed need to worry about the possibility of stigmatization and discrimination, either against or on behalf of technologically enhanced individuals. Social justice is also at stake and we need to ensure that enhancement options are made available as widely and as affordably as possible. This is a primary reason why transhumanist movements have emerged. On a grassroots level, transhumanists are already working to promote the ideas of morphological, cognitive, and procreative freedoms with wide access to enhancement options. Despite the occasional rhetorical overreaches by some of its supporters, transhumanism has a positive and inclusive vision for how we can ethically embrace new technological possibilities to lead lives that are better than well.

The discussion about transhumanism is important because it, in its essence, also deals with the part of neuroethics that pertains to brain enhancements. The making and taking of a memory pill; connecting wetware to hardware; and altering genes for non-medical purposes all deal with an aspect of transcending the naturally given about human beings. Of course, so do glasses and contact lenses. But these are mostly tobe seen as tools to help, rater than something that changes you as what you are. Cosmetic neurology (PDF document) is the term for the artificial enhancement of the brain. I'd say that the term is a bit misguided, since in my view, the "cosmetic" sounds too superficial. If you manipulate the brain, you're tinkering with what a person is per se. Taking a "brainy pill", or adding hardware parts to boost your neuronal engine goes beyond the mere tool that glasses and lenses are. There is not much of a "cosmetic feel" about it when you start changing who you are and what defines you as human: error-prone, forgetful, emotional, mortal.

So, in a way, maybe we shouldn't be too be worried about the societal aspects about cosmetic neurology (or transhumanistic thought). It is possible that cosmetic neurology is neither the problem nor solution to many of today's world's problems such as poverty and inequality between people. Nor should we think of it as something that will add much to the difference, though it will be something that might mark the difference between poor and whealthy. What we should be concerned about is how technical and medical enhancements will change how people define themselves. Just as so and so many use iPod today, will we see communities of people that start inoperating wireless communication into their brains, as in Peter Hamilton's affinity function in the Night's Dawn triolgy? IOW, we should start thinking about what "brain enhancement" does to the individual rather than staring ourselves blind at the societal problems.

-Thomas

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