Senescent microglia and astrocytes accumulate with age and disease, secreting SASP factors that amplify neuroinflammation. Senolytics have shown efficacy in murine tauopathy models. Key challenges for clinical translation include identifying the specific senescent populations driving pathology, CNS delivery, and avoiding beneficial senescent cells in tissue repair.
Senolytics targeting p16/p21+ senescent astrocytes and microglia may reduce SASP-driven neuroinflammation.