Onset, Development, and Consequences of Autonomic and Sensory Dysfunction in Autism Spectrum Disorder - PROJECT SUMMARY/ABSTRACT Atypical sensory reactivity is pervasive and highly impairing in autism spectrum disorder (ASD). Sensory reactivity contributes to core and associated ASD features, such as impaired social communication and elevated social fear, which are evident in infancy and predictive of later anxiety. Increasing theoretical and empirical data suggest that individuals with ASD may exhibit autonomic nervous system (ANS) hyperarousal at baseline (i.e., at rest), implying an elevated biological state primed for threat even during non-threatening situations. While ANS dysfunction has been posited as an underlying neurobiological mechanism contributing to specific features of the ASD phenotype, research has not examined the presence, onset, developmental trajectory, or developmental consequences of ANS function in infants at an elevated likelihood of ASD. Thus, this study proposes a longitudinal study of ANS function with data collected at 6, 9, 12, 24, and 36 months in infants at elevated likelihood for ASD given an older sibling diagnosed with ASD (EL-ASIBs) in comparison to low-likelihood infants to investigate ANS dysfunction as a potential mechanism of heterogeneity in core and associated features of ASD, including sensory processing, social communication, and social fear. The specific aims are to (1) identify the presence, onset, and developmental trajectory of baseline ANS dysfunction; (2) determine the developmental trajectory of ANS responsivity to sensory input and its relationship to baseline ANS (dys)function; and (3) identify how baseline ANS dysfunction and responsivity to sensory input predict social communication and social fear across infancy. This work will have tremendous impact by increasing our understanding of the neurobiological mechanistic underpinnings and biological pathways leading to ASD symptom progression that is essential to identify targets and timing of treatment for ASD.