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- W4200076251 abstract "Abstract Cellular senescence and inflammation are interconnected causes and consequences of tissue aging. Here, we implemented orthogonal approaches to study their interaction in steady-state mature and aged mouse brain. Using single cell sequencing, we identified a putative senescent microglial population, which increased in abundance with age and was characterized by increased expression of p16 and chemotactic senescence associated secretory phenotype (SASP) factors. Using p16-INK-ATTAC transgenic mice to eliminate p16ink4a-positive senescent cells and mass cytometry, we show that p16ink4a-positive cell targeting reduced the abundance of activated inflammatory cells in the aged female brain. Age-dependent declines in executive cognitive function were improved following transgenic p16ink4a-positive cell targeting, and executive function robustly correlated with inflammatory brain cell composition in females. Collectively, our findings demonstrate fundamental differences in the age- and sex-dependent brain inflammatory landscape and implicate p16ink4a-positive senescent cell targeting as a therapeutic strategy to attenuate age-related inflammation and cognitive decline." @default.
- W4200076251 created "2021-12-31" @default.
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- W4200076251 date "2021-12-01" @default.
- W4200076251 modified "2023-10-18" @default.
- W4200076251 title "Cell Senescence as a Mediator of Age-Dependent Brain Inflammation" @default.
- W4200076251 doi "https://doi.org/10.1093/geroni/igab046.953" @default.
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