Few robust biomarkers have been identified for autism, and there are no medications that treat the social deficits associated with the disorder. Progress has been impeded in part by the challenge of obtaining relevant tissue samples from people with autism and matched controls.

Although genetic mouse models circumvent this problem, there are difficulties in comparing complex human behavior with laboratory-based mouse behavior. These limitations underscore the value of developing a monkey model of naturally occurring social impairments with reliable behavioral and biological correlates to the human features of autism.

Karen Parker and her research team at Stanford University in California, in collaboration with John Capitanio of the University of California, Davis, and Elliott Sherr of the University of California, San Francisco, are pursuing three related goals. First, they plan to validate a statistical classification model that serves as a screening tool to rapidly identify social extremes in a large monkey population. Second, they plan to test candidate biomarkers in the cerebrospinal fluid and blood of monkeys showing low sociability.

Finally, they aim to test the genetic relatedness of the monkey model to human autism by investigating whether rare gene variants implicated in autism are found in the extremes of low-sociable vs. high-sociable monkeys. If successful, a robust monkey model of autism may be used to link abnormal social behavior with protein- and gene-based biological changes in a way that has not previously been possible.

Further development of this model may help identify novel targets for drug development, provide new blood-based metrics for treatment–response efficacy, and facilitate testing for pharmacotherapies that could benefit people with social impairments.