Autism has diverse genetic causes, most of which are still unknown. About 1 percent of people with autism have disabling mutations in a gene called Shank3, which is critical for brain development. Without a functional Shank3 gene, individuals develop typical autism symptoms including repetitive behavior and avoidance of social interactions. In a study of mice engineered to have the corresponding murine gene turned off during embryonic development, MIT researchers have now shown that they can reverse some of those behavioral symptoms by turning the gene back on later in life, allowing the brain to properly rewire itself. “This suggests that even in the adult brain we have profound plasticity to some degree,” says Guoping Feng, Ph.D., an MIT Professor of Brain and Cognitive Sciences. “There is more and more evidence showing that some of the defects are indeed reversible, giving hope that we can develop treatment for autistic patients in the future.” Dr. Feng, who is the James W. and Patricia Poitras Professor of Neuroscience and a member of MIT’s McGovern Institute for Brain Research and of the Stanley Center for Psychiatric Research at the Broad Institute, is the senior author of the study, which was published online on February 17, 2016 in Nature. The paper’s lead authors are former MIT graduate student Yuan Mei and former Broad Institute visiting graduate student Patricia Monteiro, now at the University of Coimbra in Portugal. The article is titled “Adult Restoration of Shank3 Expression Rescues Selective Autistic-Like Phenotypes.” The Shank3 protein is found in synapses — the connections that allow neurons to communicate with each other. As a scaffold protein, Shank3 helps to organize the hundreds of other proteins that are necessary to coordinate a neuron’s response to incoming signals.
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