A beta version of the brain

New products have teething problems, development bugs; they need beta development, shaking down before they are reliable. We can presume that this may also be true of the evolution of new species. The great innovations come with side-effects. I have encountered people who said this about our chronic back pains being a side-effect of upright walking. It is a great thing but may have a couple of weak spots. We would actually be surprised if evolution didn’t take some time in a shake down of a new species.


A recent paper in Cell by 20 authors (this was really a big international effort) has tackled the question of whether autism is the unfortunate result of the malfunctioning of a relatively new aspect of the human brain. The essence of the paper is given in a press release from Yale:

(the team) identified the evolutionary changes that led the NOS1 gene to become active specifically in the parts of the developing human brain that form the adult centers for speech and language and decision-making. This pattern of NOS1 activity is controlled by a protein called FMRP and is missing in Fragile X syndrome, a disorder caused by a genetic defect on the X chromosome that disrupts FMRP production. Fragile X syndrome, the leading inherited form of intellectual disability, is also the most common single-gene cause of autism. The loss of NOS1 activity may contribute to some of the many cognitive deficits suffered by those with Fragile X syndrome, such as lower IQ, attention deficits, and speech and language delays … it is a more recent evolutionary adaptation possibly involved in the wiring of neural circuits important for higher cognitive abilities. The findings of the Cell paper support this hypothesis. The study also provides insights into how genetic deficits in early development, a time when brain circuits are formed, can lead to disorders such as autism, in which symptoms appear after birth.


There are a couple of aspects that should be brought up in context of this research. First, this is unlikely to be the only cause of autism. Autism is defined as a set of symptoms (and a not too clearly specified set with arbitrary measures – not a yes/no blood test or the like). A number of causes could end up with similar symptoms. Even a number of genetic causes could end up with the same end result.


Second, when the NOS1 activity is disrupted, the brain will not simply step back to a previous version of the homo brain. We should not make the mistake of assuming that our ancestors resembled people with autism. It may be that the functions that were replaced by the products of NOS1 are no longer available.


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