Genes 2 Brains 2 Mind 2 Me

Comparisons of “healthy” vs. “disordered” genomes in psychiatry have not yet revealed sequence differences that can reliably predict the onset of mental disability.  Rather, such disability seems to arise from as-yet-undetermined complex, probablistic interactions of genetic risk and environmental factors over the course of development.  With this as the case, the demarcations between “healthy” and “disordered” may not be distinct, but rather fuzzy and hence unworthy of labels that give a false impression of being discrete states.

One recent paper that speaks to this issue is by Meyer-Lindenberg et al., “Genetic variants in AVPR1A linked to autism predict amygdala activation and personality traits in healthy humans” [doi: 10.1038/mp.2008.54].  Here, they explore genetic variation in the AVPR1A gene – a receptor for the pro-social neuropeptide vasopressin – and how it can modulate the activity of the amygdala when subjects view human faces (vs. a geometric shapes control condition).  Since it is well known that the amygdala responds to a wide range of social and emotional stimuli and that activation of the amygdala can enhance or prevent the storage of such emotional or socially arousing events – and – that this process goes awry in autism and in subjects with amygdala damage (the picture above shows that patients with amygdala damage do not focus on the eyes of human faces) – the investigators have indeed focused-in on a key set of neural processes.  They find the variation in the RS1 and RS3 polymorhphic sites in AVPR1a do indeed correlate with amygdala activity in healthy controls who were carefully screened for no history of mental disability.  A great example of folks who carry the “healthy” label, but also the genetic risk and the neural correlates of autism.