Astrocytic SIRT1 ameliorates cognitive deficits after traumatic brain injury via autophagy-mediated MEGF10 phagocytosis.

ABSTRACT: Traumatic brain injury (TBI) frequently causes cognitive dysfunction, with astrocytes playing a pivotal role in its pathogenesis. ​Specifically,​​ TBI triggers excessive astrocyte reactivity, ​leading to a phagocytic phenotype in astrocytes that contributes to abnormal synaptic phagocytosis and cognitive decline. ​Sirtuin 1 (SIRT1) reduction was region-specific, with significant downregulation observed in the hippocampus and cortex, reflecting the selective vulnerability of these regions to TBI-induced pathology. Although​ SIRT1 ​is​ a neuroprotective deacetylase, its regulatory mechanism in post-TBI astrocyte phagocytosis remains unclear. This study elucidates the mechanism through which SIRT1 attenuates TBI-induced cognitive deficits, specifically by ​​promoting autophagic flux in astroc

SUBMITTER: Ji Q 

PROVIDER: S-EPMC12755027 | biostudies-literature | 2025 Dec

REPOSITORIES: biostudies-literature