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Dr. Abrams is a Clinical Associate Professor in the Department of Psychiatry and Behavioral Sciences at Stanford University where he conducts research investigating the brain bases of social communication impairments in children with autism spectrum disorders (ASD). Dr. Abrams research focuses on understanding why children with ASD often "tune out" from the social world around them and how this impacts social and brain development. His research employs a combination of psychophysical, cognitive, and brain imaging techniques, with the goal of identifying key neural features underlying social deficits in children with ASD.Dr. Abrams received his undergraduate degree from University of Arizona followed by a period in industry as an acoustical engineer in the San Francisco Bay Area. He subsequently completed his graduate degree from Northwestern University and joined the Stanford University community as a postdoctoral researcher in 2008. Dr. Abrams joined the Stanford faculty in 2014 and was promoted to Clinical Assistant Professor in 2018 and Clinical Associate Professor in 2021.Dr. Abrams’s research program has been supported by multiple funding agencies including the NIH, NARSAD, and the National Organization for Hearing Research Foundation.Dr. Abrams lives in the Bay Area with his wife, children, and gifted Labrador retriever, Meatball.
Autism spectrum disorders (ASD) are among the most pervasive neurodevelopmental disorders and are characterized by significant deficits in social communication. A common observation in children with ASD is that affected individuals often “tune out” from social interactions, which likely impacts the development of social, communication, and language skills. My primary research goals are to understand why children with ASD often tune out from the social world and how this impacts social skill and brain development, and to identify remediation strategies that motivate children with ASD to engage in social interactions. The theoretical framework that guides my work is that social impairments in ASD stem from a primary deficit in identifying social stimuli, such as human voices and faces, as rewarding and salient stimuli, thereby precluding children with ASD from engaging with these stimuli.My program of research has provided important information regarding the brain circuits underlying social deficits in ASD. Importantly, these findings have consistently implicated key structures of the brain’s reward and salience processing systems, and support the hypothesis that impaired reward attribution to social stimuli is a critical aspect of social difficulties in ASD. The first study produced by this program of research was published in the Proceedings of the National Academy of Sciences and showed that children with ASD have weak brain connectivity between voice processing regions of cortex and the distributed reward circuit and amygdala. Moreover, the strength of these speech-reward brain connections predicted social communication abilities in these children. A second study, which was recently published in eLife, examined neural processing of mother’s voice, a biologically salient and implicitly rewarding sound which is associated with cognitive and social development, in children with ASD. Results from this study identified a relationship between social communication abilities in children with ASD and brain activation in reward and salience processing regions during mother’s voice processing. A third study, published in Proceedings of the National Academy of Sciences, showed that mother’s voice activates an extended voice processing network, including reward and salience processing regions, in typically developing children. Moreover, the strength of brain connectivity between voice-selective and reward and salience processing regions predicted social communication abilities in these neurotypical children. Together, results provide novel support for the hypothesis that deficits in representing the reward value of social stimuli, including the human voice, impede children with ASD from actively engaging with these stimuli and consequently impair social skill development. My future research will leverage these findings by examining several important questions related to social information processing in children with ASD. First, we aim to study longitudinal development of social brain circuitry in minimally verbal children with ASD, a severely affected subpopulation that has been vastly underrepresented in the ASD literature. Second, we aim to examine the efficacy of naturalistic developmental behavioral interventions, such as Pivotal Response Treatment, for children with ASD and their relation to changes in social brain and reward circuitry. Third, we aim to examine distinct neural profiles in female children with ASD who, on average, have better social communication abilities compared to their male counterparts.