Neuro death through autophagy via the acetylation of FoxO1 by SIRT2 in the hippocampus of mice in a autism spectrum disorder mice model

Autism Spectrum Disorder (ASD) is a series of complex neurodevelopmental disorders, which can affect children's social, behavioral and communication abilities. A member of the Sirtuins family of NAD + dependent deacetylases called SIRT2 could regulate the inflammation progress during stress, but the relevant mechanism has not been clearly defined. In the present study, the ASD model of wild type and SIRT2 knock out mice was established to evaluate the impact on the homeostasis of neurons in the hippocampus using western blotting, immunofluorescence and Nissl staining. The results showed that the amplification of neuronal richness was significantly decreased and neuroinflammation increased in the hippocampus following ASD due to autophagy, caused by enhancing the acetylation of FoxO1 using SIRT2 gene deletion and indicating this should be the target for ASD or other psychological stress treatment.

Automated summary

Autism Spectrum Disorder (ASD) is a complex neurodevelopmental disorder that affects children's social, behavioral, and communication abilities. This study investigated the impact of the SIRT2 gene in regulating inflammation in a mouse model of ASD. The results showed that the deletion of the SIRT2 gene led to decreased neuronal richness and increased neuroinflammation in the hippocampus, suggesting it as a potential target for ASD or stress treatment.