TSPO deficiency exacerbates acute brain damage after intracerebral hemorrhage in male mice.

ABSTRACT: Intracerebral hemorrhage (ICH) is a stroke subtype with no effective treatment despite high morbidity and mortality rates. The delineation of the mechanisms of brain damage after ICH is critical to identifying novel molecular targets for therapeutic intervention. Apart from the augmented expression of 18 kDa translocator protein (TSPO) in microglia/macrophages post-ICH and its potential to track neuroinflammation, the precise function of TSPO after brain damage remains largely enigmatic. In the present study, we employed transgenic animal models, such as global and myeloid-specific conditional knockouts, to elucidate the functional role of TSPO in ICH-induced acute brain damage. Neurological deficits, neurodegeneration, and neuroinflammation were assessed at 3-days post-ICH in male and fem

SUBMITTER: Bonsack F 

PROVIDER: S-EPMC12081391 | biostudies-literature | 2025 Sep

REPOSITORIES: biostudies-literature