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.

自闭症谱系障碍（ASD）是一种以社交和重复症状为特征的神经发育障碍。ASD 的一个关键特征是症状的早期表现，表明早期的病理生理机制。在 ASD 小鼠模型中，越来越多的证据表明存在可以及早纠正的早期病理生理机制，以防止成人的表型缺陷，克服了成人开始治疗的短期效应的缺点。此外，基因修复的结果表明，在某些情况下，即使在大脑完全成熟后，与 ASD 相关的表型也可以得到挽救。这些结果表明，我们需要在 ASD 模型研究中同时考虑时间和机制方面，并仔细比较遗传和非遗传校正。这里，