Researchers at Beth Israel Deaconess Medical Center (BIDMC) have gained new insight into the genetic and neuronal circuit mechanisms that may contribute to impaired sociability in some forms of Autism Spectrum Disorder. Led by Matthew P. Anderson, MD, PhD, Director of Neuropathology at BIDMC, the scientists determined how a gene linked to one common form of autism works in a specific population of brain cells to impair sociability. The research, published today in the journal Nature, reveals the neurobiological control of sociability and could represent important first steps toward interventions for patients with autism. “In this study, we wanted to determine where in the brain this social behavior deficit arises and where and how increases of the UBE3A gene repress it,” said Anderson, who is also an Associate Professor in the Program in Neuroscience at Harvard Medical School and Director of Autism BrainNET Boston Node. “We had tools in hand that we built ourselves. We not only introduced the gene into specific brain regions of the mouse, but we could also direct it to specific cell types to test which ones played a role in regulating sociability.”
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