Abstract
Timing and social timing deficits are fundamental in autism and may play a developmental role in its manifestation. Sleep problems are associated with this disorder, as is a reduction or loss of Purkinje cells associated with regions of the brain which co-ordinate fine motor movements. Genetic studies suggest that a number of genes of limited effect lead to autism and that the genes are epistatic. We suggest that anomalies in clock genes operating as timing genes in high frequency oscillator systems may underlie the timing deficits of autism. We outline how anomalies in methylation-related genes may also be implicated.
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