Early and Late Corrections in Mouse Models of Autism Spectrum Disorder

Autism spectrum disorder (ASD) is a neurodevelopmental disorder characterized by social and repetitive symptoms. A key feature of ASD is early-life manifestations of symptoms, indicative of early pathophysiological mechanisms. In mouse models of ASD, increasing evidence indicates that there are early pathophysiological mechanisms that can be corrected early to prevent phenotypic defects in adults, overcoming the disadvantage of the short-lasting effects that characterize adult-initiated treatments. In addition, the results from gene restorations indicate that ASD-related phenotypes can be rescued in some cases even after the brain has fully matured. These results suggest that we need to consider both temporal and mechanistic aspects in studies of ASD models and carefully compare genetic and nongenetic corrections. Here, we summarize the early and late corrections in mouse models of ASD by genetic and pharmacological interventions and discuss how to better integrate these results to ensure efficient and long-lasting corrections for eventual clinical translation.

Automated summary

Autism spectrum disorder (ASD) is a neurodevelopmental disorder characterized by social and repetitive symptoms. Studies in mouse models have shown early pathophysiological mechanisms that can be corrected to prevent phenotypic defects in adulthood. Additionally, gene restorations have demonstrated the rescue of ASD-related phenotypes even after the brain has fully matured.