We assume that the ASD etiology may be strongly associated with a synergistic eect of several epigenetic causes, which together manifest as a neurobehavioral syndrome but each independently represents only a subclin-ical, not manifest problem. According to our previous review we have found specific relations among autism, Folate Receptor Auto Antibodies and local folate disturbances in a brain.
Further research of high volume information about metabolomics, signaling, genetic coexpression, protein interactions and other information could reveal some new facts and knowledge about the multifactorial nature of ASD.