Just thought this NY Times graphic nicely captured the outlays of debt taken on during the recent weeks by the US Central Bank. Healthcare spending is usually the big item(s), but the new debt really dwarfs it. Immense new pressure on the financing of healthcare.
Posted in Uncategorized | Tagged economics | Leave a Comment »
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Amidst the current economic panic, I’m feeling more shocked than usual when listening to the flip-flopping, falsehoods, fabrications, backstepping, about-facing and unabashed spin-doctoring spewing forth from the news media. If watched long enough, one may even develop empathy for Henry Paulson who carries the weight of the global economy on his shoulders. Nevertheless, what do we know about making mistakes ? Not necessarily global financial catastrophies, but little everyday mistakes. Why do some of us learn from our mistakes ? What’s going on in the brain ? Enter Michael Frank, Christopher D’Lauro and Tim Curran, in their paper entitled, “Cross-task individual differences in error processing: Neural, electrophysiological and genetic components” [Cognitive, Affective, & Behavioral Neuroscience (2007), 7 (4), 297-308]. Their paper provides some amazing insight into the workings of human error-processing.
It has been known for some time that when you make a mistakke – oops! – mistake, that there are various types of electrical current that emanate from the frontal midline (cingulate cortex) of your brain. The so-called error related negativity (ERN) occurs more strongly when you are more focused on being correct and also seems to be more strong in people with certain personality traits (apparently not news commentators or politicians) while the error positivity (Pe) occurs more strongly when you become consciously aware that you made an error (perhaps not functioning in news commentators or politicians). Perhaps the ERN and Pe are basic neural mechanisms that facilitate an organisms adaptive ability to stop and say, “hey, wait a minute, maybe I should try something new.” The Frank et al., paper describes a relation between learning and dopamine levels, and suggests that when dopamine levels dip – as happens when our expectations are violated (“oh shit!, I bought stock in Lehman Brothers“) – that this may facilitate the type of neural activity that causes us to stop and rethink things. To test whether dopamine might play a role in error processing, the team examined a common variant (rs4680) in the catechol-o-methyl transferase gene, a gene where A-carriers make a COMT enzyme that is slower to breakdown dopamine (a bulky methionine residue near the active site) than G-allele-carriers. Subjects performed a learning task where correct responses could be learned by either favoring positive feedback or avoiding negative feedback as compared to neutral stimuli. The team suspected that regardless of COMT genotype, however, there would be no COMT association with learning strategy, since COMT influences dopaminergic activity in the frontal cortex, and not in the striatum, which is the region that such reinforcement learning seems to be stored.
Interestingly, the team found that the error positivity (Pe) was higher in participants who were of the A/A genotype, but no difference in genetic groups for the error related negativity (ERN). This suggests that A/A subjects deploy more attentional focus when they realize they have made an error. Lucky folks ! My 23andMe profile shows a GG at this site, so it seems that when I make errors, I may have a normal ERN, but the subcortical dopamine that dips as a result does not (on average) result in much greater attentional focus. Oh well, I guess its the newsmedia pool for me.
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Posted in Cingulate cortex, COMT, Dopamine | Tagged 23andMe, Dopamine, economics, Frontal lobe | Leave a Comment »
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Having a great time reading Michael Gazzaniga‘s new book, “Human – the science behind what makes us unique” and thought I’d see to what extent his conclusions might square with genetic data on population history and natural selection etc. and also evaluate my 23andMe profile to see to what extent I’m carrying the latest greatest derived alleles (more human-ish) or the older clunkier ancestral alleles.
I’ll try and keep updating this post as I work my way through the book. Here goes:
Chapter 1: Are human brains unique ?
Big Brains and Big Ideas ? (p.10) – In this section discussing how brain size may or may not relate to function and specialization of function, there are a number of genetic factors which have been linked to brain development and natural selection. Most well reported [doi: 10.1126/science.1116815] are the A44871G and C45126A variations in the ASPM gene. My 23andMe profile shows a GG and CA at these sites (rs964201 and rs3762271 respectively). Apparently, the G-allele (rs964201) and the A-allele (rs3762271) are derived, so I’m feeling very unique having scored 3/4 in this first query!
Posted in ASPM | Tagged 23andMe, evolution, Michael Gazzaniga | Leave a Comment »
Image by Colin Purrington via Flickr Just piling on to the many comments on today’s NY Times profile of David Goldstein who justifiably points out a dearth of whole-genome-snp-scanning success. One interesting debate is whether natural selection had anything to do with expunging the much sought-after (impossible to find) deleterious, disorder-promoting variants (he suggests yes) which means that whilst separate human cultures adapted to separate climate, predators, diets etc. one might expect to identify separate genetic variants that define racial or cultural subgroups (he says no). Huh?
According to the article, Goldstein “says he thinks that no significant genetic differences will be found between races because of his belief in the efficiency of natural selection. Just as selection turns out to have pruned away most disease-causing variants, it has also maximized human cognitive capacities because these are so critical to survival. “My best guess is that human intelligence was always a helpful thing in most places and times and we have all been under strong selection to be as bright as we can be.””
We have a free and open article describing the relationship of a common variant in the COMT gene with human intelligence, which is also supported by a recent meta-analysis on COMT. These findings certainly do not refute Dr. Goldstein’s conclusions, but rather make me wonder why the common valine/methionine variant in COMT might exert a tiny, but measurable, effect on intelligence. Balancing selection possibly ?
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Posted in COMT | Tagged evolution, Intelligence, Natural selection | Leave a Comment »
Image via Wikipedia You see a masterpiece while I see splatters of paint on a canvas. Why – in neural terms – do we see the same painting and feel so subjectively different ?
Understanding the neural crosstalk between visual inputs (the raw neural activity generated in the retina) and our complex internal states (needs, desires, fears etc.) of an organism is a research problem that is long on philosophy but rather difficult to address experimentally. Professors P. Read Montague and Brooks King-Casas provide a conceptual overview to how such neural crosstalk might be collected, analyzed and understood in terms of basic computational processes that underlie human decision making. In their article, “Efficient statistics, common currencies and the problem of reward-harvesting“, [doi: 10.1016/j.tics.2007.10.002] they provide an historical review of some of the major conceptual frameworks and give examples of how basic research in the area of reinforcement learning (dopamine serves as a reinforcement signal since it is released in the ventral striatum when you get more than you were expecting) might serve as a core cellular mechanism underlying the inter-linking of incoming sensory information with internal states. Dr. Montague’s book on decision making is also a fun experience & great introduction to the burgeoning area of neuroeconomics.
Posted in Dopamine, Striatum | Tagged Dopamine, Neuroeconomics | Leave a Comment »
Image via Wikipedia Just thought it was strange to see the beautiful people drooling into 23andMe spit cups in today’s “Style” section of the NY Times. Strange in a good way.
Posted in Uncategorized | Tagged 23andMe | Leave a Comment »
Image by -kÇ- via Flickr Session 4 of our discussion group, “When Basic Neuroscience Meets Psych Rehab” will meet on Sept 25. This session will cover the topic of ‘affect labeling’ which is one strategy for managing one’s emotions. Did you know there are 3,000+ words you can choose from to describe your feelings ? How many can you name right off the bat ? The discussion seeks to flesh out the way in which basic brain mechanisms of emotional regulation work and how brain-based (and genetic) biomarkers might be used in a clinical therapy/rehabilitation setting. Slides and discussion highlights will be posted to the website.
Posted in Uncategorized | Tagged Emotion, Functional magnetic resonance imaging, rehabilitation | Leave a Comment »
Image via Wikipedia Doctor David Ledbetter gives an eloquent editorial overview in his piece, “Cytogenetic Technology: Genotype and Phenotype” [doi: 10.1056/NEJMe0806570] on the renaissance underway in the field of medical cytogenetics. The use of high density arrays for genome-wide copy number variation has identified a slew of new sites showing recurrent microdeletion that are reliably found in patients with mental developmental disabilities (autism, mental retardation, schizophrenia to name a few). Ledbetter suggests that the ‘genotype first’ process of diagnosis is now much more effective with the help of the new arrays. He notes, “a pediatrician has the option of ordering this test as an adjunct to or replacement of a standard karyotype and can expect a much higher yield of clinically significant results”. This is an exciting realization of the long-awaited promise of genetics in medicine.
Posted in Chromosome structural variants | Tagged autism, Genetic testing, Personalized medicine, schizophrenia | Leave a Comment »
Image by Getty Images via Daylife A recent article in “Technology Review” profiles Austan Goolsbee, a professor at the University of Chicago School of Business & senior economic advisor to Barack Obama. I was surprised by a comment he made suggesting that as healthcare spending continues to expand, he can see it becoming a central driver of economic growth, if not, a major foundation of economic growth. Indeed, the end product of all this bioscience is much more valuable than a new car or big-screen LCD television. I’m hoping we’ll hear more on this new perspective in the coming months (and 4 years).
Posted in Uncategorized | Tagged Barack Obama, economics | Leave a Comment »
Image by pchow98 via Flickr One of the cool things about the brain & one of the ways in which it differs markedly from our current computer systems is that cells and synapses are living dynamic entities that grow and sprout new connections in response to experience. Since the 1980’s studies using protein synthesis inhibitors have shown that protein synthesis is necessary for an organism to store, recall and re-store, etc. various aspects of memory. The question for some time has been, “well, what protein(s) exactly ?” In their paper entitled, “ERK-dependent PSD-95 induction in the gustatory cortex is necessary for taste learning, but not retrieval” [DOI:10.1038/nn.2190], Elkobi et al., examine the role of PSD-95 a sort of general purpose scaffolding protein expressed in post-synaptic membranes that anchors the many molecular components that make up the synaptic machinery. They show that PSD-95 is indeed upregulated in the rat gustatory cortex after exposure to a novel stimulus (flavor) and that when it is selectively down-regulated via lentiviral expressed siRNA, that the creation of long term memories was disrupted. Interestingly, the paper shows a 3-hr time lag in the induction of PSD-95 after exposure to the memorable stimulus. Wow, that means I have 3 hours to selectively block long-term memories … I wonder what would be worth not remembering ?
Posted in PSD95 | Tagged Memory, Neuron | Leave a Comment »
Image via Wikipedia The “Central Dogma” of molecular biology rightfully points out a somewhat one-way transfer of information from DNA to RNA to protein. This mechanism has obvious implications for evolution insofar as you are issued a newly shuffled genome at birth and must make the best of it – no cheating allowed by receiving the acquired levels of fitness of your parents – since these cannot be transmitted via the bare thread of DNA. This being the case, however, it is, of course, fun to encounter ways in which mother nature skirts the rules. The term ‘mother‘ is particularly apt to the work of Michael Meaney and colleagues in Montreal, who have for many years been teasing apart mechanisms underlying maternal care in mammals. It seems that when a female rat has been deprived of good mothering (copious licking & grooming are the traits of a good rat mom) they, themselves, also demonstrate poor mothering skills (sadly, daughters DO grow up to be their mothers). The Meany group provide a great review of the mechanisms of this seeming example of “inheritance of acquired characteristics” in their review, “Epigenetic Programming of Phenotypic Variations in Reproductive Strategies in the Rat Through Maternal Care” [DOI: 10.1111/j.1365-2826.2008.01725.x]. Apparently, this mode of inheritance is dependent on the early development of neuro-endocrine circuits that regulate emotional responsivity and are dependent on early, neonatal environmental stimulation (licking & grooming activate these developing circuits) – and is not dependent on the sperm/egg-bourne passage of a particular stretch of DNA. Interestingly though, the team demonstrates that genomic CpG hypermethylation of the estrogen receptor might serve as a mechanism to maintain the effect – at the level of the genome – of the mother’s poor parenting. Mom’s who were poorly cared for as infants may have a hypermethylated estrogen receptor and therefore are more likely to demonstrate poor parenting in adulthood as a result of the maintainence of this methylated (transcriptionally repressed) estrogen receptor. More interestingly, the team has recently begun to investigate this mechanism in humans, and reported that in post-mortem analysis of hippocampal tissue from individuals who experienced early life neglect and, tragically, suffered death from suicide, that there seems to be a similar type of hypermethylation. Their PLoS ONE article, “Promoter-Wide Hypermethylation of the Ribosomal RNA Gene Promoter in the Suicide Brain” [DOI: 10.1371/journal.pone.0002085] provides an analysis of promoters of rRNA genes in the hippocampus – a brain region whose development and structure is negatively affected by environmental stress and neglect. This is a line of research that is interesting on many levels – from Lamarck to Freud. As a parent, the work shows how important it is to understand & appreciate the role of parenting and social welfare in mental health.
Posted in Estrogen | Tagged Epigenetics, Lamarck, Parenting, Suicide | Leave a Comment »
Just saw this on engadget … fun and useful – just like chumby but with a medical twist. Who knows, it may someday make housecalls (see link below).Related articles by Zemanta
Posted in Uncategorized | Tagged economics, Personalized medicine | Leave a Comment »
Image via Wikipedia Sometimes we humans tend to think we’re pretty sophisticated, but let’s face it, once we’ve got a fridge full of food and a partner to mate with, most of us – like every other species – are pretty content. So it may seem reasonable, from an evolutionary standpoint, that a gene that regulates food intake and metabolism – leptin – would have wide-ranging effects on almost every physiological system in the human body including: immune, reproduction, endocrine, skeletal and CNS. A new PLoS ONE paper entitled, “Leptin Replacement Improves Cognitive Development” reports that administration of recombinant leptin to a 5-year-old boy with a nonconservative missense leptin gene mutation (Cys-to-Thr in codon 105) yields dramatic improvements in neurocognitive function. The open access paper describes the many known effects on leptin on neuronal plasticity and it is wonderful indeed to see its success when used as a therapeutic agent. That the development of so-called ‘higher’ cognitive function in humans is regulated by a small peptide secreted by fat cells may be an affront to some, but not me. “Honey, pass the chicken wings !”
Posted in Leptin | Tagged Development | Leave a Comment »
Image via Wikipedia Siming Shen et al., in their paper, “Age-dependent epigenetic control of differentiation inhibitors is critical for remyelination efficiency“ provide insight on basic mechanisms of myelination. While myelination (think of it as the plastic insulation on copper electrical wires) makes normally developing neural networks much more efficient, it has a way of inhibiting the re-development and repair of mature neural circuits. The research team shows that recruitment of histone deacetylases (HDACs) is rather inefficient in mature oligodendrocytes precursor cells (the cells that adhere to bare neuronal axons and form the insulating myelin-rich sheath) in contrast to younger cells which differentiate readily. HDAC1 and HDAC2 are shown to down-regulate of Hes5 and Sox2, which have previously been implicated in blocking the differentiation of stem cells to oligodendrocytes. Here, the term ‘epigenetic’ refers to the mechanism of gene regulation – not by way of transcription factors binding to specific sequences – but rather, by factors being sterically blocked from binding by the 3-dimensional superstructure of the chromosome that occurs when histone proteins are deacetylated. The team suggests that as the brain ages, it becomes more difficult to recruit HDAC1,2 to the promoters needed to shut down the expression of the differentiation inhibitors. The results pose a confound for the certain applications of inhibitors of histone deacetylases (HDACi) which have demonstrated anti-tumor activity – but may – as suggested by this article – have negative consequences on brain repair processes.
Posted in HDACs, Myelin | Tagged Epigenetics, Stem cell | Leave a Comment »
Image via Wikipedia The mitogenic activities of the vascular endothelial growth factor protein family are well researched. A number of findings have linked this gene to learning and memory and hippocampal-dependent response to antidepressant medication. Indeed, its reasonable to expect that a mitogen such as VEGF would regulate hippocampal cell division and the accompanying benefits of new brain cells. Using high resolution structural MRI, Blumberg and team report evidence for such in their paper, “Influence of Vascular Endothelial Growth Factor Variation on Human Hippocampus Morphology“. Individuals with the CC genotype at rs833070 and rs2146323 – located in the intron of the VEGF-A gene displayed smaller hippocampal volumes than T-allele and A-allele carriers, respectively. These 2 snps lie in a haplotype block with rs833068 which was assayed in my 23andMe profile – indicating that I happen to carry the TT genotype at rs833070 giving me slightly larger, more neurogenic & resilient hippocampus – I suppose. Now, if I could just figure out a way to put it to good use !
Posted in Hippocampus, VEGF | Tagged 23andMe, exercise, Memory | Leave a Comment »
It has been reported that cigarettes can impart some calm and clarity from racing thoughts and mental fog. Patients with schizophrenia, who often experience cognitive disorganization, are 2-4 times more likely than the general population to smoke, and also seem to prefer stronger brands of cigarettes. This is not surprising since nicotine can raise levels of dopamine indirectly via stimulation of alpha4/beta2 high affinity nicotinic acetyl choline receptors (nAChR) expressed widely in the parietal cortex of the human brain. In an open access article entitled, “Association of attentional network function with exon 5 variations of the CHRNA4 gene“, Georg Winterer and colleagues demostrate that individuals who vary in a synonymous G/A variant (rs1044396) in the CHRNA4 gene – an snp which has previously been associated with nicotine dependence – show differential brain activity in the parietal cortex. When asked to remain alert and respond to rare visual “oddball” stimuli (visual oddball detection task), subjects with the AA genotype showed robust brain activity in the parietal cortex while subjects with the GG genotype showed very little change in activity. This finding reveals where in the brain – circuits connecting to the parietal cortex – may be especially important in mediating self-medication and even in the management of side-effects in psychiatric pharmacotherapy. Although rs1044396 is not measured in my 23andMe profile, the neighboring rs3787138 showing tight LD is measured and reveals that I am a boring, middle of the road heterozygote. As such, I do admit that I could use some mind-clearing relief from time to time – but, the yellow teeth are not quite worth it.
Posted in acetylcholine, CHRNA4 | Tagged 23andMe, Addiction, Nicotine, schizophrenia | Leave a Comment »
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Just a pointer to a great overview article of trends in medical tourism at Economist magazine. Hope the price of jet fuel doesn’t put a damper on these exciting trends.
Posted in Uncategorized | Tagged economics, medical tourism | Leave a Comment »
Image via Wikipedia Nowadays, as many folks peer into the vast tangled thicket of their own genetic code, they, as I, assuredly wonder what it all means and how best to ascertain their health risks. One core theme that emerges from repeated forays into one’s own data is that many of us carry a scads of genetic risk for illness, but somehow, find ourselves living rather normal, healthy lives. How can this be ? A recent example of this entails a C/T snp (c) located in the 5′ flanking region of the neuregulin 1 gene which has been repeatedly associated with schizophrenia. Axel Krug and colleagues recently reported in their paper, “Genetic variation in the schizophrenia-risk gene neuregulin1 correlates with differences in frontal brain activation in a working memory task in healthy individuals” that T/C variation at this snp is associated with activation of the frontal cortex in healthy individuals. Participants were asked to keep track of a series of events and respond to a particular event that happened “2 events ago” . These so-called n-back tasks are not easy for healthy folks, and demand a lot of mental focus – a neural process that depends heavily on circuits in the frontal cortex. Generally speaking, as the task becomes harder, more activity in the frontal cortex is needed to keep up. In this case, individuals with the TT genotype seemed to perform the task while using somewhat less activity in the frontal cortex, rather than the risk-bearing CC carriers. As someone who has tried and failed to succeed at these tasks many times before, I was sure I would be a CC, but the 23andMe data show me to be a non-risk carrying TT. Hmmm … maybe my frontal cortex is just underactive.
Posted in Frontal cortex, NRG1 | Tagged 23andMe, Frontal lobe, schizophrenia | Leave a Comment »
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The small neuropeptides oxytocin (OT) and arginine-vasopressin (AVP) are well known for their influence on promoting warm-and-fuzzy social behaviors in mammals. The G-protein coupled OTR and AVPR1a receptors are also the subject of much research in this area – particularly AVPR1a – since it shows differences in brain expression in polygamous vs. monogamous vole species, and also shows genetic associations with dysfunction in human social affiliation. In a recent foray into this line of research, Richard Ebstein and colleagues examine whether an individual’s willingness to give away a cache of money is related to genetic variation in the promoter of the AVPR1a. In their paper, “Individual differences in allocation of funds in the dictator game associated with length of the arginine vasopressin 1a receptor RS3 promoter region and correlation between RS3 length and hippocampal mRNA“, the researchers asked 203 college students to play the “dictator game” where, simply, one person gets a sum of money and can choose to keep it or give some of it away to the other player. Thats it. Give some of it away if you like, or just walk away with all of it, no questions asked & no consequences (your identity and the identity of the other player are masked). Amazingly, individuals actually DO give some of the money away (15% gave none of it away, 35% gave half away and 7% gave all – yes, all of it – away) … and more amazing still … those with longer stretches of microsatellite repeats at the RS1 & RS3 promoter sites in the AVPR1a gene, gave away significantly more money than individuals with shorter version of the repeats.
Posted in AVPR1a, G-protein, OTR | Tagged Emotion, Monogamy | Leave a Comment »
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Indeed, learning how to manage one’s response to the negative emotions of others and stay out of trouble is an important life skill. At some point, most of us learn to just avoid angry, mean or melodramatically negative people and save ourselves the strife. Roy Perlis and colleagues, in their recent paper, “Association of a Polymorphism Near CREB1 With Differential Aversion Processing in the Insula of Healthy Participants“, show how the transcriptional regulator CREB might exert an influence on this learning process. By having subjects view images of various facial expressions, the investigators found that individuals with the TT genotype at rs4675690 (C/T) showed less negative activation in the left insula, a brain region that is known to activate when subjects feel disgust, but not happiness, desire or fear. Subjects with the TT genotype have been shown to require more effort in the management of negative emotions and are at greater risk for suicide when being treated for depression. In the Perlis et al., study, TT subjects showed less of an effort (as measured in key presses) to avoid viewing emotionally distressing pictures. The known role of CREB in neural plasticity suggests that this gene may facilitate neural changes associated with memory. Unfortunately, 23andMe does not cover this SNP, so I’ll just have to hope that (during the upcoming election) my insula keeps me on the path to enlightenment.
Update: Thanks so very much Brian for the info on rs7591784. This explains a lot – I’m a GG here, which means I’m a TT at rs4675690 – and have always had difficulty handling it when folks are rude to me.
Posted in CREB, Insula | Tagged 23andMe, Emotion, Insula, Memory | Leave a Comment »
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