Social Neurosciences Research Program

Our Research

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 pediatric 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 studies” 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 teamparticipating in one of our research studies, or by donating to our research program.

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We are currently hiring a new assistant clinical research coordinator! For more information, click here

Dr. Parker's Faculty Spotlight

Dr. Parker Featured in Brains Behind the Institute


Recent News

Our recent study developed a primate model of naturally occurring low sociality and identified differences between low-social and high-social monkeys in neuropeptide and kinase signaling pathways previously implicated in mammalian social behavior and syndromes related to autism. Further analysis revealed that cerebrospinal fluid (CSF) arginine vasopressin (AVP) was the key marker of group differences in monkey sociality. We also found low CSF AVP concentrations in a small cohort of children with autism. These findings suggest that the AVP signaling pathway warrants consideration in future research that seeks to develop diagnostic tools and treatments for autism.