Second, identifying a genetic pattern in this way is not equivalent to identifying the effects of particular genes or gene products. As the authors point out, the twin design affords the ability to quantify, based on a standard and vetted model,

“genetic influences on complex traits that likely involve large numbers of genes and their interactions.” Nonetheless, there is ample evidence to support their claim that an aggregate selleck compound genetic effect influences cortical regionalization in humans, which is highly consistent with findings from animal studies wherein transcription factor expression was experimentally manipulated. The clear demonstration of genetic influences on human cortical regionalization has straightforward implications for evolutionary mechanisms of the expansion and functional apportionment of the cortex. The comparisons between prior www.selleckchem.com/products/DAPT-GSI-IX.html findings in mice and the current findings on regionalization in humans described by Chen et al. (2011) underscore the notion that selective pressure can influence, via an aggregation of genetic influences, the evolution of cortical development such that a “visual” species, like humans (and other primates), has a relatively greater amount of cortical resources for visual processing, whereas a “somatosensory” species, such as the rodent, has

a relatively greater amount of cortical resources for somatosensory processing. Chen et al. (2011) note similar expansions in the genetic divisions of human frontal and temporal cortex relative to rodents, which they speculate may be linked to the evolution of language and other “higher-order” cognitive processes. Several findings from the study are congruent with observations in human pathologies of cortical development. The anterior-posterior orientation of the genetic MYO10 effects are consistent with observations from human genetic lissencephalies (“smooth brain” syndromes), now well known to have severity increases or decreases along the anterior-posterior axis, depending upon

which gene is involved; DCX has greater pathology anteriorly and LIS1 has greater pathology posteriorly (e.g., Pilz et al., 1998). The observation that genetic patterning is mostly symmetric between hemispheres is consistent with the phenomenon of certain polymicrogyria syndromes, which have a strong propensity to be bilaterally symmetric and regional (Barkovich et al., 1999 and Leventer et al., 2010). The lack of genetic effects mapping onto a specific area, such as V1, is also consistent with the observation that cortical migration defects have not been demonstrated to affect a single neocortical area to the exclusion of others. These observations are also congruent with the idea that no one gene affords a neocortical area with its areal identity (O’Leary et al., 2007).