Thursday, February 28, 2008

Utter Speculation of a Neurological Sort

It seems intuitively obvious to me that the axonal projections from one part of the brain to another are approximate at best. Presumably, some gene gets turned on that leaves a trail of proteins for where the axons are supposed to go and they wind up within a centimeter or two of where they belong. Following that, the connection is actually made and refined between the two brain regions using learning and dendritic pruning.

So: This model already accounts for a large amount of the variations in personality, intelligence, and talents of otherwise normal humans. If a projection between the visual cortex and the motor cortex is off by more than a standard deviation or so, you'll wind up with somebody with poor hand-eye coordination because there will be fewer axons to make rich pattern-matches. If you wind up with more than the average number of neurons in the medial geniculate projecting into the primary auditory cortex, the likelihood might go up that you'll have perfect pitch.

But it's also reasonable to assume that the gene expression that controls these projections sometimes goes horribly wrong, causing profound deficits. My guess (and here's where the utter speculation begins) is that we see people with projection errors every day. Many of the projection errors cause subtle, possibly even undetectable, deficits. Others cause things like schizophrenia and, more importantly, autism. In fact, we know that the term "autism" covers a large number of abnormal behaviors, all of them related to some sort of abnormality in the sensory processing of information, either by the cortex or the limbic system. Might it be possible that the bulk of these defects are in fact projection errors?

We think that the incidence of autism is rising rather sharply in the population of the developed countries. All sorts of reasons for this have been proposed, many of them revolving around toxins in the environment. I can buy that argument; after all, the influence of even minute amounts of toxins on the projection markers could easily be profound.

But it is also the case that humans in developed countries are being forced to process information in novel ways. Think of the neurological stress that TV, the internet, and video games causes. For almost all of these media, processing the information presented probably makes the brain work in ways for which it hasn't evolved.

We also know that environmental stress causes epigenetic changes in individuals which are heritable. Little hunks of germ plasm DNA get methylated or de-methylated, and the zygotes that develop from that DNA will behave differently from those with "normal" DNA.

Now--and here's where I'm going way out on the limb--what if the stress of attempting these new and increasingly common modes of cognition causes enough neurological stress on the brain that epigenes get activated, which then cause the number of random projections to increase? This sounds like an excellent mechanism to produce neurological adaptation to new environmental stresses. From these random epigenetic changes, humans might eventually evolve new neural projections that process information more efficiently in response to the new cognitive stresses.

Of course, most of these changes in projections would simply result in varying degrees of cognitive damage. Only the rare projection would actually be adaptive. So, during such a spurt in environmental stress, you'd see a much higher incidence of cognitive deficits like autism, in addition to seeing a small number of people with highly adaptive talents. Once the adaptive talents spread through the gene pool, the environmental stress would abate and the number of cognitive deficits would therefore return to its normal background rate.

Note that I've made a couple of completely insupportable leaps here. First, I'm assuming that neural projection is epigenetically controllable. As far as I know, there's no evidence for this yet. The second (and more serious) guess is that there's eventually some mechanism that can code epigenetic adaptations into genetic mutations. Again, I know of no such mechanism. However, some of the evidence supporting punctuated evolution would imply some mechanism like this.

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