Dr. Mosconi completed his Ph.D. in Clinical Psychology and an APA-approved Clinical Internship at the University of North Carolina – Chapel Hill. He then performed his postdoctoral training in developmental cognitive neuroscience and pediatric neuropsychology at the University of Illinois in Chicago. Dr. Mosconi joined the faculty in Psychiatry at the University of Illinois in Chicago from 2009-2011, moved onto the faculty at the University of Texas Southwestern Medical Center from 2011-2015, and joined the faculty at the University of Kansas in August, 2015. He currently is the Director of the Kansas Center for Autism Research and Training (K-CART), Associate Professor in the Clinical Child Psychology Program, and Interim Associate Director of the Life Span Institute. Dr. Mosconi’s research is focused on sensorimotor dysmaturation and underlying brain mechanisms in neurodevelopmental disorders, including autism spectrum disorder and FMR1 related disorders. His work has been supported by NIH (NIMH, NINDS, NICHD), the Department of Defense and Autism Speaks. He has published in multiple high impact journals including JAMA Psychiatry, the Journal of Neuroscience, Journal of Neurophysiology, Molecular Autism, NeuroImage and Biological Psychiatry.
Autism spectrum disorders (ASD) represent a set of clinically and etiologically heterogeneous neurodevelopmental conditions. Clinical heterogeneity is a major challenge for understanding the diverse neurodevelopmental mechanisms that contribute to ASDs. Studies of sensorimotor behaviors in ASD hole promise for parsing this heterogeneity and clarifying basic physiology for multiple reasons. First, sensorimotor impairments are common in ASD and manifest early in development, suggesting that they may be core to the disorder. Second, the neural substrates of select sensorimotor behaviors are relatively well understood indicating that studies of sensorimotor behavior may inform neurodevelopmental models of ASD. Third, we have found that unaffected first-degree relatives of individuals with ASD show sensorimotor issues similar to probands with ASD. Examination of the familiality of sensorimotor impairments in ASD therefore may provide insights into pathogenic processes. In this presentation, studies of multiple different sensorimotor impairments in ASD and their underlying physiology will be discussed. I also will describe results from new family studies of sensorimotor behavior showing that impairments in family members may reflect risk dimensions independent of core social-communication issues. Collectively, these studies converge to suggest that sensorimotor impairments may play a more central role in ASDs than previously believed, and that analysis of their development, physiology, and familiality in ASD will provide important new information for parsing heterogeneity and clarifying pathophysiological mechanisms.