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In previous posts, I drew attention to findings linking over-activity of the pre-frontal cortex (PFC) to psychosis thanks to the imprinted brain theory's distinctive concept of hyper-mentalism. According to the theory, hyper-mentalism explains many of the symptoms of psychosis and stands in diametric opposition to the hypo-mentalism of autism, which is another way of describing the social and theory-of-mind deficits symptomatic of the disorder. The PFC seems to be critical to both, but in opposite ways: over-active in psychosis and by implication under-active in autism.
But now a new study reveals that 7 male autistic children aged 2-16 had 67% more neurons in the PFC at autopsy compared to 6 age- and sex-matched non-autistic controls. Indeed, in the dorso-lateral PFC they had 79% more! At first sight, this astonishing finding might seem to contradict the predictions of the imprinted brain theory because it seems to suggest that a larger number of PFC neurons translates into greater activity there and so--according to the theory--into hyper-mentalism, rather than the hypo-mentalistic deficits characteristic of autism. But far from contradicting the imprinted brain theory, this finding spectacularly confirms it.
The reason lies in a fundamental fact about brain development. This is that building a brain is not like building a house, where bricks and other parts are added cumulatively until the building is finished. Brain development, by contrast, is more like sculpting: there is an initial proliferation of neurons followed by selective elimination until just the right ones remain. As in the case of making a sculpture, where the majority of the stone may end up on the studio floor and only a small part of it may be retained in the finished work, so in the development of parts of the brain like the PFC: the vast majority of neurons initially produced have to be eliminated to yield the final, functional result.
If not, the outcome would be like an unfinished sculpture, only partly formed, and this is what the study seems to suggest. It implies that the mentalistic deficits symptomatic of autism and known to be associated with the PFC result from incomplete, arrested development thanks to the retention of many more neurons than normal. And of course, if that is correct, it in no way contradicts the theory.
On the contrary: another fundamental prediction of the imprinted brain theory is that autism is associated with enhanced expression of paternal genes (and/or reduced expression of maternal ones). Paternal genes like IGF2 promote growth (because paternal genes in a mammalian fetus benefit from growth at the expense of the mother, but without any cost to the father). And the fact that all fathers are male means such genes might also account for the so-called extreme male brain aspect of autism. Applied to the PFC, this would predict exactly what we find: enhanced early growth associated with later mentalistic dysfunction.
Until now, it has not been clear how growth enhancement caused by paternal genes could translate into mentalistic deficits of the kind symptomatic of autism, thanks to the fact that bigger usually means better, or at least more. But this remarkable finding suggests a completely unexpected and--in retrospect--obvious way in which this could happen. And although a single, small study like this is hardly enough to establish the principle, it is certainly enough to suggest it as a possibility that cannot be dismissed. At the very least, critics who may have scoffed at the idea of growth-enhancing genes explaining cognitive deficits will now have cause to think again, and an important precedent for future research will have been set.
Now all we need is for someone to show that the excess brain growth seen in autism is the product of paternal genes, ideally IGF2!
(With thanks and acknowledgment to Jonas Förare for bringing this to my attention.)
