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Archive for the ‘imaging genetics’ Category

In a recent review article in Nature Reviews Neuroscience, Antonio Rangel, Colin Camerer and Read Montague suggest a framework for neuroeconomic research. Indeed, the very core of its idea is simple, but not simplistic. After reading the article, I think it will provide a useful reference for future research into neuroeconomics, aka value-based decision making. I’ve made a copy of the model here for you to see:

The caption reads:

Basic computations involved in making a choice. Value-based decision making can be broken down into five basic processes: first, the construction of a representation of the decision problem, which entails identifying internal and external states as well as potential courses of action; second, the valuation of the different actions under consideration; third, the selection of one of the actions on the basis of their valuations; fourth, after implementing the decision the brain needs to measure the desirability of the outcomes that follow; and finally, the outcome evaluation is used to update the other processes to improve the quality of future decisions.

In my own emerging work on this arena, I am trying to combine this with recent advances cognitive neuroscience. First, the advances in imaging genetics, i.e., the knowledge and study of how genetic variance leads to specific changes in neurotransmission, which in turn may affect cognition, emotion and behaviour. Second, the advances in the cognitive neuroscience of ageing, i.e, the relationship between age-related changes in brain structures and functions, and mental alterations.

Briefly put, in a just submitted manuscript, I suggest that the Rangel-Camerer-Montague framework can serve as a model for looking at genotype and age effects. This leads us to three advances: first, it provides a better way to illustrate and understand the minute details of the preference and decision making systems. Second, it serves as a demonstration that individual (and intra-individual) differences must be taken into account. The “economic agent” is not a homogenous subject, but an agent that differs from person to person and with persons over time. Finally, it may also serve as a framework for identifying potential ways to induce alterations in the systems, e.g., through medical intervention. More on this story later, given that the manuscript is accepted 😉 For now, here’s an illustration of how genotype (exemplified through COMT, MAO-A and 5-HT) and age effects may expand the model. Of course, this is only scratching the surface, but I hope you’ll see what I mean.

This is an extended version of the Rangel-Camerer-Montague model. Within each processing node, two dimensions are added, here exemplified with the three primary nodes. The genotype dimension is a categorical variable that divides subjects into two or three classes, while the age dimension is continuous (inset, top left).

-Thomas

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imaging-genetics.jpgThe third annual conference on imaging genetics was held at Irvine this January. Neither Thomas nor I could go this year, but people tell me it was just as great as previous years. Now you can tell for yourself: videos of all the presentations can now be watched via this web-site. Among the speakers are Lisa Eyler, David Goldstein, Steven Potkin, and Andreas Meyer-Lindenberg.

-Martin

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gal507.jpgThe next International Imaging Genetics Conference is opening its doors now for registration. The third year in a row, building on two successful conferences, this third meeting will also house two separate workshops: one on brain imaging for geneticists; and one on genetics for brain imagers. All in the spirit of crossing the bridge between genetics, brain imaging and statistics. As this course was brilliant last year, I’m hoping to attend in January 2007, too.

Here is the announcement:

The First and Second International Imaging Genetics Conferences were held to bring together national and international experts in neuroimaging, genetics, data-mining, visualization and statistics. Targeting physicians and scientific researchers, this annual conference features presentations from investigators world-wide and held in-depth discussions within the emerging field of Imaging Genetics. Given the known importance of both genetics and environment in brain function, and the role of neuroimaging in revealing brain dysfunction, the synergism of integrating genetics with brain imaging will fundamentally change our understanding of human brain function in disease. To fully realize the promise of this synergy, we must develop novel analytic, statistical, and visualization techniques for this new field.

This international symposium was held to initially assess the state of the art in the various established fields of genetics and imaging, and to facilitate the transdisciplinary fusion needed to optimize the development of the emerging field of Imaging Genetics. The Third Annual International Imaging Genetics Conference will be held on January 15th and 16th, 2007 at the Beckman Center of the National Academy of Sciences in Irvine, CA. We look forward to seeing you at this exciting upcoming event.

Monday January 15th:

  • Nicholas Schork, UCSD “Multivariate Analysis of Combined Imaging and Genomic Data”
  • Eleazer Eskin, UCSD “Analysis of Complex Traits Through Intermediate Phenotypes.”
  • Tom Nichols, University of Michigan “Statistical Challenges & Opportunities in Imaging Genetics”
  • Fabio Macciardi, University of Toronto “Integrating Imaging Genetics Methods in Schizophrenia.”
  • David Goldman, NIAAA “Genes and Neurobiologies in the Addictions”
  • David Goldstein, Duke Institute for Genome Sciences and Policy “Neuropsychiatric pharmacogenetics”
  • Daniel Weinberger, NIMH/NIH: TBA

Tuesday January 16th:

  • Joseph Callicott, NIMH “Does risk for schizophrenia arise from multiple genes in vulnerable pathways? Evidence from DISC1 and FEZ1”
  • Lisa Eyler, UCSD “Genetics of Brain and Cognition: A Twin Study of Aging”
  • Fei Wang, Peking University “Neuregulin 1 Genetic Variation and anterior cingulum integrity in schizophrenia and in health.”
  • Andreas Meyer-Lindenberg, NIMH/NIH “Genetic characterization of prefrontal-subcortical interactions in humans.”

**New for 2007** Sunday January 14th:

*** Half-day Workshop tutorials will be offered the day before the conference at the Beckman Center- see website for details***

Workshop 1: What Geneticists need to know about Brain Imaging
Workshop 2: What Brain Imagers need to know about Genetics

Registration and conference information can be found at the conference website

-Thomas

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brainimagingbehavior.jpgIt’s not every day that we see a new journal emerging. However, Springer now launches a new journal called Brain Imaging and Behavior. According to the mission statement, the goal of the journal is to

publish innovative, clinically-relevant research using neuroimaging approaches to enhance the understanding of neural mechanisms underlying disorders of cognition, affect and motivation, and their treatment or prevention.

In this sense, the journal seems to have the ultimate goal of disease understanding and treatment. However, as they write, research on individual differences in representation of normal functions is important as well. What I find particularly interesting is that “brain imaging” is taken to imply a whole range of imaging methods in the study of the brain. It involves everything from the higher cognitive functions to molecular imaging methods. This implies the different approaches that involves genetics, behaviour and neuroimaging, AKA imaging genetics.

Brain Imaging and Behavior sounds like a very interesting initiative. I had problems finding the first online articles (this link). And would it not be better if the journal, just as any science journal, was free? It would be good if they followed the example of PLoS.

-Thomas

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Avshalom Caspi and Terrie Moffitt [interview with Moffitt here on npr] made quite a splash in 2002 when they published the paper “Role of Genotype in the Cycle of Violence in Maltreated Children” in Science. They reported that maltreated children would differ in the development of antisocial personality and violent behaviour depending upon whether or not their genotype conferred high or low levels of MAOA expression, a neurotransmitter-metabolizing enzyme. Thus, Caspi and Moffitt showed that a genetic variation may moderate the influence of environmental factors on behaviour in a rather dramatic manner, fueling the growing suspicion that the old nature/nurture dichotomy is much too simplistic. Behaviour is most probably not determined by either an innate genetic Bauplan or the ever changing forces of our surroundings. In Caspi and Moffitt’s study, at least, children with a low-level MAOA genotype only developed an antisocial personality if maltreated (if you happen not to be maltreated, a low-level MAOA polymorphism will not cause you to develop an antisocial personality); but, at the same time, maltreatment doesn’t affect children with a high-level MAOA polymorphism, so the maltreatment is not a cause in itself either. Genes and environmental factors interact to produce behaviour, and the real question is how they do so.

In the July issue of Nature Reviews Neuroscience Caspi and Moffitt discuss some important implications of their research. First of all, if you wish to understand how external pathogens can influence the brain, as is all-important for psychiatric treatment, you have to factor in the individual person’s genetic make-up. The ability of environmental factors to alter the nervous system and generate a disordered mind variates with genetic differences at the DNA sequence level. Say Caspi and Moffitt:

Heterogeneity of response characterizes all known environmental risk factorsfor psychopathology, including even the most overwhelming of traumas. Such response heterogeneity is associated with pre-existing individual differences in temperament, personality, cognition and autonomic physiology, all of which are known to be under genetic influence16. The hypothesis of genetic moderation implies that differences between individuals, originating in the DNA sequence, bring about differences between individuals in their resilience or vulnerability to the environmental causes of many pathological conditions of the mind and body.

Secondly, to really understand this interaction of genes and environmental risk factors and pathogens, more epidemiological cohort studies must integrate neuroscience measurements. As Caspi and Moffitt observe:

First, evidence is needed about which neural substrate is involved in the disorder. Second, evidence is
needed that an environmental cause of the disorder has effects on variables indexing the same neural substrate. Third, evidence is needed that a candidate gene has functional effects on variables indexing that same neural substrate. It is this convergence of environmental and genotypic effects within the same neural substrate that allows for the possibility of gene–environment interactions. At present, such evidence concerning environmental and genotypic effects in relation to neural substrate measures is sparse, and therefore gene–environment interaction hypotheses are likely to be circumstantial at best, and flimsy at worst. But this situation is steadily improving. When we were constructing our hypothesis regarding the genetic moderation of the depressogenic effects of stressful life events, we were aided by direct evidence linking the 5-HTT candidate gene to individual differences in physiological responsiveness to stress conditions in three different experimental paradigms, including knockout mice, stress-reared rhesus macaques and human functional brain imaging.

Of course, imaging genomics studies, such as those by Hariri and Weinberger, or Meyer-Lindenberg, give a good idea of how genetics, brain activity and behaviour can be related to each other, using avant-garde research techniques.

Finally, both perhaps most intriguing, Caspi and Moffitt suggest that findings such as theirs indicate that genes react to environmental influences more than cause brain activity and behaviour. This stance is captured in a quote like this one:

[The] gene–environment interaction approach differs fundamentally from the ‘main-effect approaches’,
with regard to the assumptions about the causes of psychiatric disorders. Main effect approaches assume that genes cause disorder, an assumption carried forward from early work that identified single-gene causes of rare Mendelian conditions. By contrast, the gene–environment interaction approach assumes that environmental
pathogens cause disorder, and that genes influence susceptibility to pathogens. In contrast to main-effect studies, there is no necessary expectation of a direct gene-to-behaviour association in the absence of the environmental pathogen.

Clearly, as such experimental work in greater detail furnish us with a more precise view of genes build the molecular structure of the brain, and how these structures underlie behaviour, we will also become better suited to settle long standing philosophical issues, such as what innateness actually is.

Reference

Caspi, A. & Moffitt, T. (2006): Gene-environment interactions in psychiatry: joining forces with neuroscience. Nature Reviews Neuroscience 7: 583-590.

-Martin

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motherbrain1.jpgHaving a baby has a large impact on how we live our lives (trust me). But whereas men may react with amazement, wonder, even jealousy of being left aside, little actually happens to our bodies after birth. The changes that happen in women are far more obvious, not only during pregnancy but after birth also. The production of milk, and the possibility of conditional learning of milk production to the child’s crying is just one example of how body, brain and mind get tuned into caretaking.

Furthermore, studies of oxytocin, a mammalian hormone that acts as a neurotransmitter in the brain, has been implicated in the bonding of the mother-infant attachment bond. Oxytocin is present in both sexes and is thought to be involved in social bonding, stress-reduction and orgasm, just to mention some. but the hormone seems to play a specific role in how mothers react to their newborns, and the establishment of a sound dyadic attachment. In this way, the brains of mothers change, both as a result of hormonal expression (loads of additional oxytocin) and the social interaction with the infant.

But did you know that some of the neurons in mothers’ brains actually stem from their babies? In other words: some of a mother’s brain cells are actually from the offspring.

This is just what a team of researchers from Singapore have found and published in the journal Stem Cells. It’s well known in this literature that fetal cells can enter the blood of circulation during pregnancy and remain there for many years after birth. These cells can, just as regular stem cells, develop into different kinds of tissue, including bone marrow, liver an spleen cells. But whether these cells can cross the blood-brain barrier has been less certain.

stemcell.jpg

The expression of fetal stem cells in the mother’s cortex at 4 months after birth. Figure 1-H from the article.

This is exactly what the researchers found. By labelling fetal stem cells they discovered that these cells had indeed crossed the blood-brain barrier and moved into the brain. Furthermore, at measurement four days after pregnancy these cells had developed into neurons, astrocytes, oligodendrocytes or macrophage-like cells. In other words, they developed just as any other stem cell.

So babies gets into their mothers’ minds in more than through hormonal and psychological mechanisms.

However, what is actually the function of these neurons is more unclear. Does the workings of fetal neurons have any significance for their relationship, or any particular mental function in mothers? This is indeed an opening field, and an eye-opener to many people (including myself when I first read it). No results have been reported in either direction as of yet.

What has been studied, however, is how these fetal stem cells can actually play a supporting role in the mother’s brain in the case of pathology. In addition to documenting that fetal stem cells enter the mother’s brain, the researchers added a condition involving brain lesion of the mother’s brain. What they found was just as surprising: after a lesion to the brain, more fetal cells were found in the lesioned region. So the baby’s cells seem tuned into helping the mother regain herself in the case of injury.
Mind-blowing as this finding may be, little is still known about this phenomenon. The development, mechanism, function and evolution of this process is just beginning to be explored. But it already raises a whole range of questions: can we measure a difference between mother’s and “non-mother’s” brains, both structurally and functionally? Does this “fetomaternal microchimerism” lead to any advantages (i.e. survival) in mothers? What is the range of variation in this kind of expression: are there “good” and “bad” fetuses? Are mothers of many children better off in any respect of those with fewer children? Or is this process just a question of striking the energy balance, the child “paying back” what it deprived the mother of during pregnagcy?

So a portion of yourself resides somewhere in your mother’s brain (and body). Children are indeed the result of their parents, but now it seems that children pay back, too.

-Thomas

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violent-child.jpgViolence and criminal behaviour is today thought to involve a series of complex interactions between heritable and environmental factors. Centuries of debate of the relative contribution of nature and nurture have not reached anything resembling a solution, and even today we can find ardent proponents and defenders of each extreme view (see Steven Pinker on this, PDF).

While violence and crime has been part of all recorded history, the society’s understanding of the underlying causes of these acts and how they should be dealt with have changed over time. In modern times, we also see a wide variety of legal practices in dealing with criminals and violators: from the death penalties and multiple life sentences in the US, Russia and other countries, to briefer treatment sentences in Europe. These different societal solutions build – explicitly or implicitly – upon what causes violence and criminal acts, and how they should, if at all possible, be treated.

It would be no understatement to claim that the biological explanation of violence and crime has not been fully implemented (nor understood) by law makers or enforcers. Just as you could say about the society in general: aside from specific demonstrations of how violent offenders have larger or smaller neural damage, little is known about the biological properties of violence. Not that the literature has been flourishing with articles demonstrating such relationships. It hasn’t. Until now, where recent studies report detailed analyses of how genes and environments alter the brain’s workings to make people more or less prone to violence, impulsive acts and criminal behaviour.

In a most interesting paper (PDF) published in PNAS, a team of researchers from Austria, Italy and USA headed by Andreas Meyer-Lindenberg have uncovered neurobiological factors that contribute significantly to violence in humans. The team studied the normal allelic variation in the X-linked monoamine oxidase A (MAOA) gene, a gene that has also been shown to be associated with impulsive aggression in humans and animals.

In the study both structural and functional MRI methods were applied. First, the researchers asked whether the low expression variant of MAOA, known to be associated with increased risk of violent behaviour, would predict differences in the size of limbic structures such as the amygdala. Indeed, what they found was that the low expression MAOA predicted limic reductions, as can be shown from the figure article

maoa-1.jpg

Structural reductions in limbic and paralimbic regions due to genotype. The size of both the amygdala and cingulate cortex are predicted by benotype. The low expression MAOA have significantly reduced volumes of these structures, compared to the high expression MAOA group.

Second, the team studied how these structures worked using two fMRI paradigms. The first task was a facial expression matching task, a task known to involve the amygdalae. The amygdala activation was significantly influenced by genotype: the low MAOA group displayed higher amygdala activation and at the same time lower activation in cingulate cortex subregions, as well as left orbitofrontal cortex and left insular cortex – all brain regions implied in emotion processing.

maoa-2.jpg

Regions involved in facial expression matching (click image for larger version). As you can see from the graphs, there is a genotype-by-gender interaction.

The second task was an emotion memory task, where subjects were asked to encode and recall aversive (compared to neutral) valenced information. Here, the results pointed to a significant genotype-by-gender interaction effect, in that men with a low MAOA version showed increased reactivity of the left amygdala and hippocampus during recall. No such relationship was found for women.

Interestingly, the researchers also found a tight relationship between gender and genotype during the first volumetric study. Here, low-MAOA males showed increased orbitofrontal volume bilaterally, while no such relationship was found in females. In this sense, the MAOA allelic variances seem to influence males most.

Finally, Meyer-Lindenberg and his co-workers draw the lines to other studies relating MAOA variance to a highened sensitivity in low-MAOA males to aversive events (e.g. abuse) during childhood. The combination of a low-MAOA genotype with such events seem to produce abnormal regulation (through the cingulate) of the amygdala and an increased predisposition to impulsivity and violence. As the authors note:

Predisposition to impulsive violence by means of abnormal activation and regulation of emotion-related amygdala function might be further enhanced by deficient neural systems for cognitive control, especially over inhibition, the capacity to suppress prepotent but inappropriate behavior that might originate from a dysregulated affective response. Although the rostral cingulate is key to the regulation of acute affective arousal and emotional learning, inhibitory control of prepotent cognitive responses is thought to be critically dependent on caudal aspects of anterior cingulate. Our study of genetic influences on cognitive impulse control revealed a sex-dependent impairment in precisely this area of cingulate, affecting men only. Our finding of a genotype-by-sex interaction in this region therefore provides a plausible neural mechanism for reduced cognitive inhibitory control in risk allele-carrying males, suggesting synergistic impairment in cognitive and emotional neural regulatory mechanisms that might render MAOA-L men at especially high risk for a neural phenotype that plausibly relates to the slightly greater probability of impulsive violence.

Endnote: it might be useful to note that this study was conducted on healthy, non-criminal volunteers. The obvious step next is to study crime offenders (different types) and the complex interplay between genes, gender and childhood events.

-Thomas

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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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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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Gene-hyped as we are here at BrainEthics, I'm mentioning a few articles that are highlighting the relationship between genes, brain and mind. As neuroscience deals with the wet matter of the mind – the fatty, information-processing and massively energy consuming body part we call the brain – we must also realize that the basic building block of the brain is the genome.

This is not as simple as it may sound. Genes simply do not merely encode how a cell is to look like or function. Genes only react to the environment in which they are situated. The development of, say, a hippocampal cell is not encoded in the genome per se; it stems from the influence of the local environment of that part of the brain, and how the brain cell (at the developmental stage actually more like a stem cell) migrates and connects to the network that will develop into the hippocampus. Neuroscience is certainly sorting out the nitty-gritty details on this, with the fantastic work by people such as Pasco Rakic. IMHO, even neuroimaging cannot escape this turn: we must move from the "blobology" of fMRI, PET and all other neuroimaging methods (this even applies to the clever diffusion fMRI, as described recently), and towards a better understanding of what goes on within these blobs. Just as I briefly mentioned in my post about Nikos Logothetis.

So here's a few additions in the story about imaging genetics, the study where neuroimaging is informed by genetic variations:

What is the hidden structure of the genome? The human genome is much more diverse and dynamic than what one could get the impression of through normal genotyping studies. Variations abound, and in a number beyond what we normally think. These are not just curiosities; they play important roles in the way that the body (and brain) develops and functions. In a news article in Nature, Andrew Sharp briefly presents two ways to study the genome, and how the new insight about variability influences current research. From the article: "The genetics community is only just beginning to appreciate the extent of structural variation present in the human genome and its role in human disease. Although we now have a finished human genome sequence in hand, geneticists have begun to appreciate that this is in fact a highly dynamic structure. The realization that the long-awaited reference sequence represents only one version of the human genome, which has significant large-scale variation between any two individuals, means that techniques such as these for investigating genome structure will be in high demand."

What is a gene? In another Nature news article, Helen Pearson discusses how RNA is becoming the new field of studying how genetic information is implemented in the organism. From the article: "In classical genetics, a gene was an abstract concept – a unit of inheritance that ferried a characteristic from parent to child. As biochemistry came into its own, those characteristics were associated with enzymes or proteins, one for each gene. And with the advent of molecular biology, genes became real, physical things – sequences of DNA which when converted into strands of so-called messenger RNA could be used as the basis for building their associated protein piece by piece. The great coiled DNA molecules of the chromosomes were seen as long strings on which gene sequences sat like discrete beads. This picture is still the working model for many scientists. But those at the forefront of genetic research see it as increasingly old-fashioned – a crude approximation that, at best, hides fascinating new complexities and, at worst, blinds its users to useful new paths of enquiry."

How heritable is Alzheimer's Disease? According to a study by Margaret Gatz and colleagues, the influence of genetics is very high, and higher than often thought. For a best-fit model estimation, genes are though to be responsible for 79%. Environmental risk factors do indeed play a role, but not as high as we might think from previous reports.

How to read the genome and its functional implications? Simon Fisher and Clyde Francks have a nice review in Trends in Cognitive Science on the genetic influence of dyslexia. Dyslexia is being used here as a model to explain how to use genotyping in a meaningful way to study the genetic influence on cognitive function and dysfunction.

These are just to mention a few important articles from this burgeoning scientific field. More are bound to follow, and we'll cover them the best we can here at BrainEthics.

(BTW, the image used here is from the Rakic Lab, illustrating the migration of brain cells during development. At the Human Brain Mapping conference in Toronto last year, Rakic held a superb talk showing movies of migrating cells. It was a true eye-opener to those of us who had not realized how much actually goes on during development. I can see that they are setting up a page for a media gallery, hopefully that will cover some of these excellent movies. I'll be watching that page closely.)

-Thomas

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