11-13-2007, 03:07 PM
The previous thread started by Autistic_Shoes got me thinking...
I theorized that a mutated "neurological patterning" gene is the root of ASDs - one copy results in Aspergers while two results in more "classic" autism. Since once copy of the mutant gene which produces Aspergers can also frequently produce socially beneficial traits, the gene has been selected for rather than against.
To take the idea further, I think that the gene may not be involved in specific neurological wiring, but rather in the patterning of brain wiring. And that changes in the gene cause a more random patterning as opposed to the more common pattern found in most NTs. The random patterning is what produces such a wide array of cognitive and sensory changes in people with ASDs and why it is so hard to "classify" ASDs, "classic" autism, Aspergers, etc.
These are the main areas that I think are involved:
I - sensing. Typical patterns produce a mixture of visual/auditory/tactile (the main ones) sensing. Random patterning will produce some combination of enhanced sensing and decreased sensing (simplistically, maybe there are 3 wires and rather than one in each plug, 2 go into the same area and one area is left with no wire or maybe 3 go in the same area and 2 are left with no wire...Alternatively, there may simply be more wires but they don't all go to the typical places.)
II - cognitive processing. Typical patterning will produce a mixture of visual/verbal/math processing functions. But, similiar to sensing above, random patterning produced changes with increased cognition in some areas and less in others.
III - communication. This may be largely a result of I and II, but also may be separately influenced by neuronal patterning. The ability to form and control speech, emotions, and motor/muscle movement could also be subject to the same random patterning processes.
If this hypothesis is true, then it should be possible to "diagnose" ASDs more definitely by assessing skills in these areas. An "average" score could be determined with a large cross-section of presumed NTs (who would still have some minor variations across the areas). ASDs would have significant increases in some areas and deficits in others. The specific areas would not matter, but rather the pattern of large shifts in sensing/cognitive/communicative abilities.
An interesting corellary to the above hypothesis is that other neurological conditions like dyslexia, OCD, ADD/ADHD, Tourettes etc could be the result of similiar changes in wiring, but involve specific wires or a specific subset of wires. In contrast, ASDs involve patterning of large groups of wires hence the broader array of effects and the frequent overlap.
I theorized that a mutated "neurological patterning" gene is the root of ASDs - one copy results in Aspergers while two results in more "classic" autism. Since once copy of the mutant gene which produces Aspergers can also frequently produce socially beneficial traits, the gene has been selected for rather than against.
To take the idea further, I think that the gene may not be involved in specific neurological wiring, but rather in the patterning of brain wiring. And that changes in the gene cause a more random patterning as opposed to the more common pattern found in most NTs. The random patterning is what produces such a wide array of cognitive and sensory changes in people with ASDs and why it is so hard to "classify" ASDs, "classic" autism, Aspergers, etc.
These are the main areas that I think are involved:
I - sensing. Typical patterns produce a mixture of visual/auditory/tactile (the main ones) sensing. Random patterning will produce some combination of enhanced sensing and decreased sensing (simplistically, maybe there are 3 wires and rather than one in each plug, 2 go into the same area and one area is left with no wire or maybe 3 go in the same area and 2 are left with no wire...Alternatively, there may simply be more wires but they don't all go to the typical places.)
II - cognitive processing. Typical patterning will produce a mixture of visual/verbal/math processing functions. But, similiar to sensing above, random patterning produced changes with increased cognition in some areas and less in others.
III - communication. This may be largely a result of I and II, but also may be separately influenced by neuronal patterning. The ability to form and control speech, emotions, and motor/muscle movement could also be subject to the same random patterning processes.
If this hypothesis is true, then it should be possible to "diagnose" ASDs more definitely by assessing skills in these areas. An "average" score could be determined with a large cross-section of presumed NTs (who would still have some minor variations across the areas). ASDs would have significant increases in some areas and deficits in others. The specific areas would not matter, but rather the pattern of large shifts in sensing/cognitive/communicative abilities.
An interesting corellary to the above hypothesis is that other neurological conditions like dyslexia, OCD, ADD/ADHD, Tourettes etc could be the result of similiar changes in wiring, but involve specific wires or a specific subset of wires. In contrast, ASDs involve patterning of large groups of wires hence the broader array of effects and the frequent overlap.