Abstract

A large share of the population-attributable risk of ASD is traceable to complex polygenic inheritance. The ability to clinically distinguish inherited from noninherited forms of ASD has significant public health implications and underscores the opportunity to complement the discovery of gene-based therapeutic targets with that of: 1) early phenotypic targets that index polygenic liability; and 2) common “comorbidities” that exacerbate the severity of impairment in ASD.

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