mirror neuron theory -- all fogged up

OK, that's a terrible pun, but it is so frustrating trying to understand all the research. Am I the only one who has been utterly convinced by the many that every child with autism has something wrong with his mirror neurons?? And yet, proving again how we do not know that which we think we know, today I read this summary of another recent study ... suggesting that after all, there is nothing wrong with the mrror neurons.

Neanderthal genes?!?

Many months ago I read what I considered to be kind of a weird essay I found on the web in which the author argued that many traits we consider to be autistic are, in actuality, remnants of Neanderthal genes. He (or she?) argued that Neanderthals had interbred with humans, and that this accounted for certain differences in some individuals. I dismissed it as pretty far-fetched.

Until this morning, that is -- when I read this Washington Post article that in fact researchers have apparently proven that Non-African humans did in fact interbreed with Neanderthals, and that except for those of us with African ancestry, between 1 and 4% of our genes can be traced to the Neanderthals.

And -- at least one of those genes -- CADPS2 -- has been linked to autism. Here's what my less than exhaustive search turned up about CADPS2 (from this article):

CADPS2 (also called CAPS2) encodes a protein that regulates the trafficking and release, or exocytosis, of vesicles containing cargo such as neurotrophic factors, which influence brain cell maturation and survival. To determine whether the absence of CADPS2 influences autism development, the researchers generated mice carrying a disrupted version of CADPS2.

The mutant mice exhibited normal visual, auditory, olfactory and motor function, all of which are normal in autistic patients. [EDITOR'S NOTE: I am astonished to read this. In my experience, most autistic children are impaired in at least some of these functions. I don't see how this is consistent with the sensory processing component of autism. Surely most of us have experience these issues in our children?] However, like autistic humans, CADPS2-deficient mice engaged in fewer social interactions with other mice, displayed heightened anxiety and reduced exploration in unfamiliar environments, and were hyperactive even in familiar surroundings.

Absence of CADPS2 resulted in cellular defects mirroring those frequently observed in the brains of autistic patients, such as reduced development and impaired survival of certain varieties of brain cells including some GABAergic interneurons and cerebellar Purkinje cells. Provision of brain-derived neurotrophic factor (BDNF), a protein found in CADPS2-associated vesicles in normal mice, rectified these cellular abnormalities.

I don't know what that means, but I guess it's time for me to learn to be a little more open-minded.