Social Neurosciences Research Program
The principal goal of the Parker Lab Social Neurosciences Research Program at Stanford University is to better understand the biology of social functioning using an integrative, translational approach. Our behavioral research spans studies of individual differences in rhesus monkey social development to studies of social cognition impairments in various clinical populations (e.g., in children with autism; in survivors of hypothalamic-pituitary tumors; in adults with posttraumatic stress disorder). We are also developing several innovative monkey models of social impairments, including studies of rhesus monkeys that naturally exhibit social cognition deficits and common marmoset monkeys which are engineered to do so. Our biological studies employ epigenetic, gene expression, and neurotransmitter-based approaches to identify biomarkers of impaired social functioning, and we also conduct treatment trials to test the efficacy of novel pharmacotherapies to improve social abilities in low-social monkeys and in children with autism. Our lab is particularly interested in testing whether “social” neuropeptide (e.g., oxytocin and arginine vasopressin) signaling pathways are implicated in human and non-human primate social behavior, and whether these neuropeptide pathways are robust biomarkers of, and treatment targets for, social impairments in clinical populations.
Please visit our “research” page to learn more about the specific projects our team is currently conducting, and ways in which YOU can help move research forward, either by joining our research team, participating in one of our research studies, or by donating to our research program.
Our study showed that 0-3-month-old infants later diagnosed with autism had significantly lower cerebrospinal fluid vasopressin concentrations compared to those who did not later receive an autism diagnosis. Infant cerebrospinal fluid vasopressin concentration also individually identified autism cases with high precision in this one-of-a-kind archival collection. These findings extend our prior cerebrospinal fluid vasopressin research conducted in behaviorally symptomatic children to suggest that a biomarker of autism may be present very early in life, before behavioral symptoms emerge. If replicated, this approach could transform how autism is detected, both in behaviorally symptomatic children, and in infants at risk for developing it. These findings were published in Proceedings of the National Academy of Sciences.