Association of Polygenic Liability for Autism With Face-Sensitive Cortical Responses From Infancy

Autism is a heritable condition affecting 1% of people worldwide. Despite a pressing need for early intervention, the developmental paths through which genetic variants are associated with emerging behavioral symptoms in infancy remain opaque. The latency of the N170 event-related potential response to faces is replicably altered in individuals with autism1 and has potential as a stratification biomarker for prognostic social functioning.2 The N170 precursor (N290) to faces vs nonfaces is also altered prior to symptom emergence in infants subsequently diagnosed with autism.3 These early differences in brain processing represent a plausible developmental mechanism linking genetic liability and behavioral autism symptoms. We investigated whether N290 latency to faces vs nonfaces is associated with autism polygenic scores and cross-disorder polygenic scores in infants with and without a family history of autism.