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Social timing, clock genes and autism: a new hypothesis
Author(s) -
Wimpory D.,
Nicholas B.,
Nash S.
Publication year - 2002
Publication title -
journal of intellectual disability research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.941
H-Index - 104
eISSN - 1365-2788
pISSN - 0964-2633
DOI - 10.1046/j.1365-2788.2002.00423.x
Subject(s) - autism , clock , gene , neuroscience , autism spectrum disorder , psychology , biology , epistasis , genetics , circadian clock , developmental psychology
Background 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. Conclusions 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.