Some disparate threads may start to come together in addition to the materials cited in the introduction.


1. Patterson's work at Caltech showing immune stimulation during a critical period of gestation results in autism like brain and behavior changes in mice. These are the same as changes due to thalidomide in a critical period of human gestation (days 20-23 post conception) corresponding to mouse induction of autism. (Similarly, misoprostol and the cited Valproic acid.)
http://www.its.caltech.ed...
http://www.plosone.org/ar...
(Other papers. See: http://www.its.caltech.ed... )


2. A class of molecules was recently discovered to be some of the most powerful anti-inflammatories known through the 5-HT2a receptor.
http://jpet.aspetjournals...
http://www.plosone.org/ar...
I know of one case of major fetal dosing with LSD, but it did not result in autism, rather the reverse.


3. Fluoxetine is anti-inflammatory, most likely through the 5-HT2a receptor. http://www.biomedcentral....


4. Pardo shows evidence for ongoing inflammation in the brains of people with ASD. http://informahealthcare....


Thus, it makes sense that there are multiple causes. Part of that is that a drug that in adults has anti-inflammatory effect could be compensated for during gestation, setting the baseline higher.


I think it likely that a 5-HT2a receptor acting anti-inflammatory molecule may fit into autism therapy by restoring the environment of the brain to settings compensated for during gestation.