Anti-inflammatory treatment rescues memory deficits during aging in nfkb1-/- mice.
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ABSTRACT: Chronic inflammation is a common feature of many age-related conditions including neurodegenerative diseases such as Alzheimer's disease. Cellular senescence is a state of irreversible cell-cycle arrest, thought to contribute to neurodegenerative diseases partially via induction of a chronic pro-inflammatory phenotype. In this study, we used a mouse model of genetically enhanced NF-κB activity (nfκb1-/- ), characterized by low-grade chronic inflammation and premature aging, to investigate the impact of inflammaging on cognitive decline. We found that during aging, nfkb1-/- mice show an early onset of memory loss, combined with enhanced neuroinflammation and increased frequency of senescent cells in the hippocampus and cerebellum. Electrophysiological measurements in t
SUBMITTER: Fielder E
PROVIDER: S-EPMC7576267 | biostudies-literature | 2020 Oct
REPOSITORIES: biostudies-literature
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