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Day 184 - Halfway!
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I’ve heard of mind reading – yes, some folks have actually figured out (here, here, here) how to decode the fMRI signal to literally know what you’re thinking – but am now beginning to wonder where it all ends. In their new paper, “Transcription MRI: A New View of the Living Brain”, by Liu and colleagues [doi: 10.1177/1073858407309746], they describe the use of short oligonucleotides that can hybridize to mRNA transcripts and, due to the presence of a paramagnetic linker on the oligo, also be visualized in the MR scanner.  This is a new technique and the paper runs it alongside more traditional reporter-gene methods (requiring post-mortem tissue however) to validate the specificity and precision of the approach.  Presently, the method is not safe for humans, so only mice need worry about who is looking at their deepest gene expressions.

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John Maynard Keynes {{ru|Джон Мейнард Кейнс}} ...
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Many folks would agree that money is not the route to happiness.  But, lets be honest, when some of your money is taken from you and just given to someone else – well now, that sure enough, has a way of pissing you off !  Such is a common refrain today, as taxpayer funds (your money) are used by Congress to bail out large banks and corporations, not to mention any number of people who irresponsibly bought mc-mansions they could not afford.  Increasingly, there is a disconnect between what people “feel” and policy recommendations based on the cold, hard, complex, econometric, quantitative financial models used to justify these so-called bailouts.  “It just feels wrong, but the experts tell us its for the best“.  Strong medicine ? Hmmm.

John Maynard Keynes (pictured here) used the term ‘animal spirits’ to describe shifts in human mood that could have unpredictable effects on market behavior.  In his recent podcast/lecture from the London School of Economics, Professor Robert Shiller opines further on these types of disconnects – those that exist between cold and dry economic models and real-life warm and fuzzy humans who inhabit a world constrained by these models that do not buffer against boom & bust cycles.  Notably, Shiller, who is now highly in demand, was widely ignored during the last great disconnect – the one where people felt so good while the stock market and housing market inflated to levels that defied sound economic models (interestingly, he remains puzzled by our new Treasury Secretary, Timothy Geithner, who also never conceded that anything might be wrong with the financial system during the pre-bust years at the Federal Reserve Bank of New York – how could he miss it ?).  Perhaps if we improved the economic models, then we could smooth-out the booming & busting ?

Shiller argues for a more flexible and sophisticated financial system that can better account for some of the emotional and social biases that make homo economicus such a greedy, panicky and yet often selfless and generous creature.  Rather than static, fixed contracts, he suggests products that can function to hedge against what he calls, “psychological contagion”.  Presently, he has created a number of such helpful products including securities which can hedge against the movement of house prices (via his Case-Shiller index) and newer securities (in development) that carry no counter-party risk and are somewhat less bubble-prone.  He also advocates more research to connect financial engineering with behavioral finance which should help develop more advanced economic models that account and quantify discrete types of social and emotional biases that arise in the marketplace.

In any case, it is clear from listening to Shiller, and from his previous books, that financial engineering is best used as a tool to help everyday folks manage the inherent uncertainties of life over the long run (in contrast to financial engineering for the purposes of creating illusory wealth bubbles).  I’m certainly a fan of Robert Shiller and wonder how basic brain science and behavioral finance might help his already groundbreaking work on the construction of financial instruments that factor-in the innate behavioral (sometimes irrational) biases that people have in assessing risk and making decisions based on long-term rather than short term outcomes.  There must be many – and even some that are influenced by genetic factors.  The new fields of neuroeconomics and its synthesis with behavioral genetics might, one day, even allow me to hedge against my own genetic risk (I carry 2 copies of the DRD4 7-repeat VNTR which, apparently, is associated with a 25-50% increase in risk taking).

My parents intuitively understood this somehow – they wisely gave me an allowance.

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Steven Pinker on Open Source
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A great article (here in the NYTimes magazine) on one psychologist’s reaction to his genome and the new consumer genomics.

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Clonidine
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A recent report by Katayama and colleagues [doi 10.1038/mp.2008.97] shows that the the gene slitrk1 – a known risk factor for the developmental disorders  Tourette’s syndrome and trichotillomania gives rise to increased levels of noradrenaline when the gene is inactivated in a developing mouse model.  In the U. S., the most frequently prescribed medications for these disorders are clonidine hydrochloride (Catapres®) and guanfacine (Tenex®), which inhibit the synaptic transmission from presynaptic nerve terminals that express the alpha 2-adrenergic receptor.  Thus, the mouse model (mice with the inactive slitrk1 gene were healthy but showed behavioral abnormalities that were normalized upon treatment with clonidine) seems to validate the current form of treatment since a reduction in noradrenergic release, might counteract the higher levels of noradrenaline associated with the risk-promoting slitrk1 mutation.

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OK, there’s not really a “coolest” part of the brain, but, some areas are pretty darn weird & wild.  Consider the cingulate cortex (shown here).  Electrical stimulation of the pACC region in humans can produce overwhelming fear – even a feeling that death is imminent – while stimulation of white matter tracts adjacent to area 25 can relieve treatment resistent depression. Activity in the MCC region is often associated – not with emotion – but with motor planning and selection of actions.  Stimulation of this area evoked the feeling of “I felt something, as though I was going to leave.” Interestingly, this region also contains a unique type of large neuron known as a von Economo cell,  found in humans and Bonobo chimpanzees, but not other primate species – leading some to speculate that this area must contribute to something that makes us uniquely human.  The PCC and RSC regions seem to be involved in how your brain computes where you are in 3-dimensional space, since activity in the PCC rises when participants mentally navigate pathways and routes of travel or assess the “self-relevance” of sensory stimuli, while lesions in RSC lead to topographic disorientation.  Whew, that’s a lot of functionality !  Indeed, with so many functions, its not surprising that this region is often linked to mental illness of all sorts.  In schizophrenia, for example, patients have difficulty controlling their actions (MCC regions have been implicated) as well as their emotions (ACC regions have been implicated) and maintaining a coherent sense of “self” (PCC & RSC regions have also been implicated).

Since we know that this brain region is implicated in mental illness and we know that mental illness arises – in part – due to genetic risk, it is of interest to begin to understand how genetic factors might relate to the development of structure, connectivity and function of the 4 sub-regions of the cingulate cortex.  With this in mind, it was great to see a recent paper from Brent Vogt and colleagues at the Cingulum Neurosciences Institute [doi: 10.1002/hbm.20667] which has begun to examine differential gene expression in these 4 subregions !  They examined the expression of an array of neurotransmitter receptors (at the protein level actually) and asked whether the expression of the receptors was able to differentiate (as lesions, activity and architectonics do) the 4 subregions.  In a word – yes – with the ACC region showing highest AMPA receptor expression and lowest GABA-A receptor expression.  This was very different from the MCC region which had the lowest AMPA receptor expression while PCC had the highest cholinergic M1 receptor expression.

This seems a great foundation for future studies that will continue to dissect the many interconnected – yet separable – functions of the cingulate cortex.  The “holy grail” of which might be to understand the evolutionary origins of the von Economo cells which are unique to our human lineage.  The genome encodes the story – we just need to learn to read it aloud.

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Drawing of Purkinje cells (A) and granule cell...
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If you like gardening, the doldrums of winter can be dreary indeed. Although I’d never admit to it, my neighbors might swear to having seen me outside strangely (pathetically) counting the number of branches on my icicle-laden roses and rhododendrons.  In any case, I do admit to spending way too much time forlornly staring at my garden from the window while fantasizing about all the things I’ll plant come springtime.

Each new branch brings a new burst of color and fragrance and concomitant joy.  A good thing right ?  Similarly, each neuron in the brain – which look just like little trees with branches – should also strive to send out as many new branches and make new synaptic connections.  Afterall, there are brain disorders associated with a loss of or fewer dendrites, such as Down’s syndrome and schizophrenia. More branches, more synapses, more brain power and concomitant joy ? Well, perhaps not quite.

A gene known as seizure-related gene 6 (sez6) which is expressed in the developing brain as well as in response to environmental stimulation, seems to play a role in limiting the the number of branches that a neuron can send out.  Gunnersen and colleagues [doi: 10.1016/j.neuron.2007.09.018] show that mice that carry an inactivated version of sez6 show more dendritic branches (implying that the normal function of the active gene is to inhibit branch formation), and that this is definitely not a good thing.  These sez6(-/-) mice, while looking rather indistinguishable from their normal littermates, did not perform as well on tasks involving motor control, memory and emotional sensitivity (implying that having too many branches may not be so beneficial).  In humans, a frameshift mutation involving an insertion of a C residue at position 1435 of the cDNA is associated with febrile seizures, similarly suggesting that dendritic overload can have negative effects on human brain function.

Clearly, the human brain seeks a balance between too many and too few dendritic branches.  I suppose most experienced gardeners would also agree that too many branches is not desirable.  Perhaps they are right.  However, I don’t think I’d mind much if plants came with an analogous sez6 mutation !

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Yankee Doodle
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Commuting to work is a total drag.  Commuting to work in New York City is not just a total drag, but THE definitive commuting nightmare.  Still, when one ponders the masses of people (more than 2 million each day) who tread in, out and around Manhattan, its pretty remarkable that one can get in to work and home again.

Consider then, the human brain, with 100 billion neuons and 1,000 trillion synapses – all of which need constant tender loving care and maintenance to keep firing along.  In some cases, the commute to these synapses can be quite long – even for a molecule (eg. if a motor neuron were as wide as my car, the commute from the nucleus to the presynaptic membrane would be about 10 miles, which is about how long I must travel to get to work).  Is the brain better able to transport cargo from home (the nucleus where lots of the basic materials are produced) to work (synaptic membranes which carry out information transfer) ?

I certainly hope so.  But, like my own commute, it seems the human brain can have commuting nightmares of its own.  One of the main transport vehicles in the brain is a molecule called Kinesin which literally walks (see the movie below) along microtubule tracks and delivers its cargo in little molecular satchels called protein transport vessicles.  One of the components of these transport vessicles, a protein known as piccolo,  is expressed in presynaptic zones and may be important for recycling presynaptic vessicles – as well as mental health.

Indeed, what might happen if the normal process of vessicle transport and synaptic maintenance were disrupted in the brain – a commuting debacle of sorts ? Well, Sullivan and colleagues [doi: 10.1038/mp.2008.125] report that a genome-wide association study of major depressive disorder yields piccolo (PCLO) as one of its major findings.  The single nucleotide polymorphism rs2522833, which encodes a serine to alanine substitution near the calcium binding region (amino acid #4814) of PCLO was one of the most significant findings in the original study and a follow-up of a different case/control population study on major depressive disorder. The change from alanine to serine is notable, since the addition of N-acetylglucosamine to serine residues is a common mechanism for regulating intracellular traffic.

My 23andMe profile shows an AA for this site, which is the serine/serine form of PCLO (the form which can be modified by GlcNA  -yay!) rather than the alanine/alanine form. This (A) allele is indicated as the major allele by the authors although the AA genotype is less common among individuals of European and Asian ethnicity, but quite common in sub-Saharan Africa.  The authors don’t reveal which allele is associated with an increased risk of depression, but I already know the answer – I’ll never recover from the depression of my own commuting nightmare.

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Aplysia_californica.
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One of the weird things about chronic pain is that it can sometimes be more “in your brain” than, say “in your back” or “in your elbow“.  Take for example, a phenomenon known as phantom limb pain – where individuals who lose a limb, can still complain of feeling pain in that very missing limb.  As described here, it is possible to “unlearn” this pain – which is a learning process involving changes in synaptic connectivity in the brain.

Where then, and how, might pain and learning related to chronic pain be happening “in your brain” rather than in your back or elbow. Well, a recent paper from Min Zhuo’s lab at the University of Toronto have reported some new insights into synaptic mechanisms of pain.  In their recent paper [doi:10.1186/1744-8069-4-40], “Enhancement of presynaptic glutamate release and persistent inflammatory pain by increasing neuronal cAMP in the anterior cingulate cortex” they evaluate the role of presynaptic glutamamte release in a brain region known as the anterior cingulate cortex – a region whose activity is well-known to correlate with reports of pain.

One of the cool tricks they used to evaluate the role of pre- vs. post-synaptic actions of glutamate was to use mice that carry a G-protein coupled receptor from the sea slug (Aplysia) which can respond to octopamine (a chemical not normally found in mouse brains) to activate glutamate release pre-synaptically.  When mice were administered octopamine in the cingulate cortex, became more sensitive to chronic pain.  This identifies a very specific biochemical pathways and brain area for which pharmacologic and behavioral therapeutics might be designed for the treatment of chronic pain.

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The visual dorsal stream (green) and ventral s...
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One of the longstanding puzzles of brain development is why, in some cases, individuals with developmental disabilities sometimes show enhanced function, rather than a more typical loss of cognitive function.  In the case of Williams Syndrome – which is caused by a hemizygous deletion of a cluster of about 25 genes on 7q11.23 – children show a mild form of mental retardation but also a notable increase in gregarious and social behaviorHow might a genetic deletion lead to a gain of function ? In a recent paper by Sarpal and colleagues [doi:10.1093/cercor/bhn004], they explore the role of the visual cortex and its role in feeding and filtering information to emotional  regions of the brain.

From its receipt of visual information from the eyes – say perhaps, you’re looking at someone’s face, the primary visual cortex parses information into 2 separate streams – a dorsal stream which is good at processing “where” information related to location; and a ventral stream which is good at processing “what”information related to identity and recognition – and moreover, provides inputs to the prefrontal and amygdala (brain regions which are important for social behaviors). What if the genes deleted in Williams Syndrome altered the development of a part of visual cortex that participates in early visual processing to alter the relative balance of dorsal to ventral processing ?  Might it result in a an individual who was better than usual at processing objects (faces) and also showing related emotional traits ? Indeed, this has been a longstanding hypothesis that has since been supported by findings that show relatively intact ventral stream processing but disrupted dorsal stream processing.

In their current paper, Sarpal and colleagues measured brain activity as well as correlations of activity (connectivity) between brain regions as patients with WS passively viewed visual objects (faces and houses).  They report that connections from early visual processing areas (fusiform and parahippocampal gyrus) in WS are actually weaker to the frontal cortex and amygdala.  Since activation of the frontal cortex and amygdala are associated with inhibition and fear, it may be case that the weaker connections from early visual areas to these regions gives rise to the type of gregarious and prosocial (a lack of fear and inhibition) behavior seen in WS.   In further pinpointing where in the brain the genes for WS might be causing a developmental change, the authors point to the ventral lip of the collateral sulcus, an area situated between the fusiform and parahippocampal gyri.  This may be the spot to more closely examine the role of genes such as LIMK1 – a gene that participates in the function of the actin cytoskeleton (an important process in synaptic formation).

This lecture by V.S. Ramachandran covers some of these pathways with respect to Capgras Syndrome.

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Economy of American Samoa
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Click here to listen to the free NPR podcast: “Uwe Reinhardt, professor of economics and public affairs at Princeton University, calls the health care sector the “strongest economic locomotive working for us.” He estimates that by 2015, health care will be one-fifth the size of the U.S. economy and says this is a good time to expand health insurance coverage for the uninsured.”

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Lollipop-Nosed
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“There is a sucker born every minute”, were the words that looped through my mind on the long train ride home after losing $200 in an unfortunate encounter with a card shark over on Canal Street, many years ago.  I recall that when the card shark (actually a kindly old man) suggested to me that I would easily outwit him and $$ win $$, I have to admit that I really, sort of, well, believed him.  Hmmm, what a sucker indeed.  Come to think of it though, he didn’t even know that I was a GG homozygote at rs4570625 in the tryptophan hydroxylase-2 gene, which according to Furmark and colleagues,  is “a significant predictor of clinical placebo response“.  Lucky for him I guess.

There is actually a lot of mainstream neuroscience research on the placebo response – for good reason – it has a way of complicating & inflating the cost of clinical trials for many neuropsychiatric disorders, but also shows that “overt suggestions” and non-medication-based talk therapies can lead to outcome improvement.  In any case, whether you prefer medication or non-medication modalities of treatment, there is much to be gained from understanding the basic biology of the placebo response. A great review on the biology of the placebo response can be found here.

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nothing like hot coffee to wash down a bite of...

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I was irked to see, in today’s New York Times, a picture of a young child having his cheek swabbed so that his parents could ascertain his status at the rs1815739 C/T variant .  T-alleles at this site give rise to a premature stop codon in the alpha 3 actinin (ACTN3) gene while the C-allele encodes a full-length protein that contributes to the fast twitching of muscle fibers.  Not surprisingly, it was found [PubMed Central ID: PMC118068] that folks who have achieved status as Olympic caliber sprinters are more likely to carry the C-allele than ethnically matched controls. The company, Atlas Sports Genetics is now marketing the test, for $149 as a means to “predict a child’s natural athletic strengths”.  Holy Crap !

Its sad to think of the myriad of ways in which genetic information can be misused and misrepresented – sadder still to think of using genetic tests to deny kids the simple joy of playing with each other.  Parents may be intersted to know that among europeans and asians, the C-allele is present at about 50%, making 75% of the population either a C/C or a C/T … which, taken alone, explains very little of why a handful of individuals achieve athletic success. Parents considering paying the $149 might also wish to read a recent article by Dr. Jerome Kagan, a well-regarded developmental psychologist on recent trends in overparenting.

My 23andMe profile shows a middling C/T which is on par with my middling soccer skills.  Nevertheless, I had a great experience learning and building relationships with my pals on the soccer field, many who remain friends decades hence.

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Flash circuit

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A recent paper from Andreas Heinz and colleagues (doi: 10.1038/nn2222) provides more neuroimaging evidence in humans for a a circuit that regulates our responsivity to stimuli that evoke emotional responses.  The basic circuitry involves the amygdala (a place in the brain where emotional memories are registered), the prefrontal cortex (a part of the brain that is involved in making decisions and assessing threats) and the cingulate cortex (a place in the brain where expectations are compared to sensory inputs & outgoing responses).  These 3 brain regions are interconnected in a loop through various synaptic contacts and the responsivity of these synapses can be modulated by neuomodulators such as dopamine, serotonin and noradrenaline.  It turns out, that several neuroimaging studies have begun to demonstrate that this (relatively) simple circuitry underlies human personality and temperament. In the Heinz study, the level of dopamine that was released into the amygdala was correlated with levels of functional activation to emotional stimuli as well as a dimension of temperament known as negative affect.

I recall once having taken the Meyers-Briggs assessment in graduate school and had a blast comparing my results with my wife – who was almost my polar opposite. Now, the latest neuroimaging and imaging-genetic research has begun to explain the complexities of human personality in basic neural circuitry where genes such as 5HTT and MAOA ‘turn up’ or turn down’ the gain on various synaptic contacts in this circuit – leading to the immense, yet systematic variation in personality and temperament that makes our social lives so interesting.  As I navigate my way through marriage and parenthood, I’m often glad I took the personality test with my wife many years ago.  It always helps to see things from the other person’s perspective.  Now, as she obtains her 23andMe profile, perhaps we will begin to compare our genomes together – the ultimate form of marriage counseling !!  Click here for more personality tests.

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Example of a subject in a Ganzfeld experiment.

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As the great J. B. S. Haldane once quipped, “The universe is not only queerer than we imagine; it is queerer than we can imagine.”  So why not delve into the outer reaches of our inner mental life.  Better yet, its Free and Open, thanks to the special issue of Cortex dedicated to recent studies on “Neuropsychology of Paranormal Experiences and Beliefs“.  Yours truly has a token article that gropes for a genetic basis for brain mechanims involved in belief formation.  Lots of fun.

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California Quail

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Am just working up a review on the genetic regulation of the noradrenergic system and stumbled across a collection of papers from ye olde 1980’s. A scientist named Nicole Le Douarin has a series of papers performing a surgical switcheroo of neural tube & neural crest cells from the quail into the chick.  Apparently, the cells survive and differentiate into mature structures and (because the quail cells were distinguishable by Feulgen stain) were a great way to study the effects of “genes vs. environment” on the development of specific cell types. Noradrenergic cells, it turns out can be induced to express cholinergic proteins in response to external cues for example. Interestingly, the chicks born with quail transplants crowed like quail, rather than chicks, demonstrating “the first demonstration of cross-species behavioral transfer brought about by neuronal transplantation.” Balaban et al., Science magazine (1988) vol 241, page 1339.

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imaging-genetics_graph

Just playing around with Joe D‘s new PubMed analysis tools – Thanks Joe ! My own area of research involves linking genetic data to functional neuroimaging data to begin to understand how genetic variation influences neural network dynamics and cognitive development in general. The term “imaging-genetics” was initially used for this purpose at the first Imaging-Genetics conference in 2005 and since then. I like the figure generated by Joe’s term trending tool since it shows the early blips of activity in this nascent field.

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U.S.

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re-posting from NARSAD news … FDA approves an amazing new form of non-invasive magnetic brain stimulation for treatment resistant depression.

Great video demonstrates the methodology and its ability to interfere with neural processing with a high degree of temporal and spatial specificity.  A new treatment that one day might be guided by genomic markers ? Perhaps.

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My Promethease Unbound

Vulcan Chaining Prometheus, Rijksmuseum, Amsterdam

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Thanks so very much to the folks at SNPedia for developing and sharing the Promethease analysis tool. What a delight to delve into my 23andMe profile ! I stumbled onto the usual dreary risks for this and that, and yes, I know I’m at risk for baldness, but did come up with a few bonus IQ points and moreover an allele that protects me from cannabis dependence (will have to return to Nijmegen sooner than later I suppose).

Just a sampling from the report … what’s in YOUR genome ?

rs2165241(T;T)  >10x increased risk of exfoliation glaucoma (LOXL1)
rs2180439(T;T)  2x increased risk of baldness
rs1136287(T;T)  3.9x increased risk of wet age related macular degeneration (PEDF)
rs1426654(A;A)  probably light-skinned, European ancestry
rs601338(A;A)  resistance to Norwalk virus infection
rs324650(A;T)  somewhat higher IQ (CHRM2)
rs1815739(C;T)  mix of sprinting & endurance muscles (ACTN3)
rs16891982(C;G)  if European, 7x more likely to have black hair (SLC45A2)
rs806368(C;C)  lower risk of the development of substance dependence
rs1954787(T;T)  ~10% less likely to respond to citalopram (HTR2A)
rs17822931(C;T)  wet earwax
rs237025(A;A)  MET/MET increased diabetes susceptibility
rs6449213(T;T)  ~4x higher risk for hyperuracemia
rs1015362(C;C)  2-4x higher risk of sun sensitivity if part of risk haplotype (ASIP)
rs1800497(G;G)  A2/A2 bupropion effective (DRD2)
rs363039(A;G)  2+ IQ points (SNAP25)
rs2383207(A;G)  increased risk for heart disease
rs2987983(G;G)  increased risk for prostate cancer
rs1800955(C;C)  increased susceptibility to novelty seeking (DRD4)
rs2279744(G;G)  generally more cancer prone (MDM2)
rs10260404(C;C) rs10239794(C;C) haplotype strongly associated with ALS
rs283413(A;C)  3.2x higher risk for PD (ADH1C)
rs1024611(G;G)  increased risk of exercise induced ischemia (CCL2)
rs1328674(T;T)  higher risk for RA (HTR2A)
rs2107301(A;A)  2.47x higher risk for prostate cancer
rs1801270(A;C)  increased risk for lung cancer
rs1571801(T;T)  >1.36x risk for prostate cancer
rs1799724(C;T)  weak risk for Alzheimer’s Disease
rs733618(C;T)  1.87x risk for myasthenia gravis (CTLA4)
rs7480010(G;G)  increased susceptibility to Type II Diabetes
rs3018362(A;A)  increases susceptibility to Osteoporotic fractures
rs4870044(T;T)  increases susceptibility to Bone mineral density variations
rs806380(G;G)  protection from cannabis dependence
rs17696736(G;G)  associated with type-1 diabetes

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Day 191 - Stick it Out

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Like “Joe the Plumber” (whose real name is Samuel), CNTNAP2 (whose real name is CASPR2) has achieved a bit of fame lately.  While recently appearing almost everywhere (here, here, here) except FOX News, CNTNAP2 (not Joe the Plumber) is apparently a transcriptional target of the infamous FOXP2 “language gene” – so says Sonja C. Vernes & colleagues [doi: 10.1056/NEJMoa0802828] who precipitated DNA-protein complexes using anti-FOXP2 antibodies from a cell line transiently expressing FOXP2. The team later evaluated measures of expressive and receptive language abilities and nonsense-word repetition and found that a series of snps – most significantly rs17236239 – were associated with performance of children from a consortium of families at risk for language impairment.  This adds to several previous reports of CNTNAP2 and risk for autism, a disorder where language ability is severely impaired.

So what’s all the fuss ? How can something so insignificant (rs17236239 not Joe the Plumber) stir up so much trouble ?  Well, as reported in a previous post, the expression of CNTNAP2 in the developing superior temporal cortex may be a relevant clue since this brain region is activated by language tasks.  Also, this gene encodes a rather massive protein which (as reported by Coman et al.,) seems to participate in the establishment of myelination and “nodes” that permit rapid neural transmission and long-range coordination across neural structures in the brain. Interestingly, this gene shows evidence for recent positive selection in humans (as posted on here and here) although the newly derived G-allele at rs17236239 seems to be the allele that is causing the language difficulties.  My own 23andMe profile shows a middling A/G here which makes it slightly hard to recall and repeat “Samuel Wurzelbacher”.

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Dodged this baldness snp

Pygargue à tête blanche / Bald Eagle

Image by meantux via Flickr

Just was skimming an article (Prodi et al., doi: 10.1038/jid.2008.60) on genetics of baldness and happened to notice that one snp mentioned is covered by 23andMe and so I, while unfortunately mostly (are there levels?) bald, felt my last few follicles stand up and cheer for my C-allele at rs1385699 in the EDA2R gene.

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