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Drug target identified that may increase social interaction in autism

A missing gene in the brain was linked to social avoidance in people with autism, and treating it may help improve the symptom of the disorder.

Researchers at the University of Pennsylvania linked a missing gene in the brain to social avoidance among people with autism spectrum disorder, and in mice missing the gene were able to correct for the symptom using drug treatment. Photo by pathdoc/Shutterstock

PHILADELPHIA, Sept. 9 (UPI) -- A gene in parts of the brain responsible for development and maintenance may represent a new drug target that could increase social interaction in people with autism, according to recent research.

Researchers at the University of Pennsylvania found in experiments with mice that compensating for the absent gene in mice born without it using a drug treatment turned autism spectrum disorder patients' social avoidance into typical social behavior, according to a study published in the journal Biological Psychiatry.

Behavioral symptoms in people with autism spectrum disorder are partially linked to lackluster connections between neurons, though researchers largely still do not understand actions, or lack thereof, in the brain causing the symptoms.

Previous genetic studies have implicated the gene protocadherin 10, or PCDH10, which is a neural cell adhesion molecule involved in brain development and the proper function of synapses. In brain regions where the protein is typical expressed, including parts of the amygdala -- which is involved with emotion and motivation.

For the study, the researchers first observed mice with the PCDH10 gene knocked out, which showed reduced social behavior similar to that seen in human ASD patients.

The researchers also saw lower levels of glutamate receptor subunits, or NMDA recepted subunits, in the amygdala. When they treated these deficits with the drug d-cycloserine, which binds to the NMDA receptor, the social avoidance seen in mice without the PCDH10 gene disappeared and they became more normal in their social interactions.

In addition to suggesting more study should be done on correcting deficits caused by the missing gene, the researchers say preliminary clinical studies with humans have shown results similar to those seen in the new study with mice -- suggesting more work should be done in the area.

"This research could significantly change our understanding of the causes and brain changes in autism and could lead to new treatment approaches for the harder-to-treat social aspects of ASD," Dr. Edward Brodkin, an associate professor of psychiatry and director of the Adult Autism Spectrum Program at the University of Pennsylvania, said in a press release.

Stephen Feller,  Sept. 9, 2016