Preclinical studies indicate an age-associated accumulation of senescent cells across
multiple organ systems. Emerging evidence suggests that tau protein accumulation, which
closely correlates with cognitive decline in Alzheimer's disease and other tauopathies,
drives cellular senescence in the brain. Pharmacologically clearing senescent cells in
mouse models of tauopathy reduced brain pathogenesis. Compared to vehicle treated mice,
intermittent senolytic administration reduced tau accumulation and neuroinflammation …