Or should we say how little?
As an interesting aside to “Neanderthals could speak, but why is it really a problem?”, there’s been a bit of publicity lately about scientists supposedly finding the “genius gene”:
Researchers have found that teenagers who had a highly functioning NPTN gene performed better in intelligence tests.
It is thought the NPTN gene indirectly affects how the brain cells communicate and may control the formation of the cerebral cortex, the outermost layer of the human brain, also known as “grey matter”.
Previously it has been shown that grey matter plays a key role in memory, attention, perceptual awareness, thought and language.
It’s quite possible that intelligence will turn out to be driven in large part by epigenetics, the critical question of how, when, and where genes are expressed or silenced. See, for example, “Epigenetics: Inheritance of acquired traits gradually gaining acceptance.”
If you think that worth considering, you won’t be surprised to learn this:
But the genetic variation identified in this study only accounts for an estimated 0.5% of the total variation in intelligence.
Surprising there was even a signal then. The finding may prove more useful in th study of genetic factors in mental illness.
Paper (no paywall). Here’s the abstract:
Despite the recognition that cortical thickness is heritable and correlates with intellectual ability in children and adolescents, the genes contributing to individual differences in these traits remain unknown. We conducted a large-scale association study in 1583 adolescents to identify genes affecting cortical thickness. Single-nucleotide polymorphisms (SNPs; n=54?837) within genes whose expression changed between stages of growth and differentiation of a human neural stem cell line were selected for association analyses with average cortical thickness. We identified a variant, rs7171755, associating with thinner cortex in the left hemisphere (P=1.12 × 10-7), particularly in the frontal and temporal lobes. Localized effects of this SNP on cortical thickness differently affected verbal and nonverbal intellectual abilities. The rs7171755 polymorphism acted in cis to affect expression in the human brain of the synaptic cell adhesion glycoprotein-encoding gene NPTN. We also found that cortical thickness and NPTN expression were on average higher in the right hemisphere, suggesting that asymmetric NPTN expression may render the left hemisphere more sensitive to the effects of NPTN mutations, accounting for the lateralized effect of rs7171755 found in our study. Altogether, our findings support a potential role for regional synaptic dysfunctions in forms of intellectual deficits.
Hat tip: Daniel Quinones
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