Restoration of Shank3 gene activity in adult mice aids recovery from some neurodevelopmental deficits, but not others

A longstanding question in neurodevelopmental biology has been whether, or to what degree, traits resulting from neurodevelopmental disorders might be reversible.

In a study published this week in Nature, a team led by Guoping Feng of the McGovern Institute for Brain Research at MIT and the Stanley Center for Psychiatric Research at Broad Institute, McGovern’s Yuan Mei, and Broad’s Patricia Monteiro, looked at mice born with impairments to Shank3, a gene known to contribute to a subset of autism cases. By reactivating the gene at different times of development, the researchers found that certain behavioral abnormalities caused by the impairment to Shank3, such as social deficits and repetitive behaviors, could be rescued even in adulthood, while other traits, such as anxiety and motor coordination deficits, could only be rescued early in development. The findings inform our understanding of brain plasticity and suggest that therapeutic interventions for neurodevelopmental disorders may be more effective if delivered early in development. Read more about their findings in MIT News.