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Cellular senescence is a state of irreversible cell\u2010cycle arrest, thought to contribute to neurodegenerative diseases partially via induction of a chronic pro\u2010inflammatory phenotype. In this study, we used a mouse model of genetically enhanced NF\u2010\u03baB activity (<jats:italic>nf\u03bab1<\/jats:italic><jats:sup>\u2212\/\u2212<\/jats:sup>), characterized by low\u2010grade chronic inflammation and premature aging, to investigate the impact of inflammaging on cognitive decline. We found that during aging, <jats:italic>nfkb1<\/jats:italic><jats:sup>\u2212\/\u2212<\/jats:sup> 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 the hippocampus of <jats:italic>nfkb1<\/jats:italic><jats:sup>\u2212\/\u2212<\/jats:sup> mice <jats:italic>in vitro<\/jats:italic> revealed deficits in gamma frequency oscillations, which could explain the decline in memory capacity. Importantly, treatment with the nonsteroidal anti\u2010inflammatory drug (NASID) ibuprofen reduced neuroinflammation and senescent cell burden resulting in significant improvements in cognitive function and gamma frequency oscillations. These data support the hypothesis that chronic inflammation is a causal factor in the cognitive decline observed during aging.<\/jats:p>","DOI":"10.1111\/acel.13188","type":"journal-article","created":{"date-parts":[[2020,9,17]],"date-time":"2020-09-17T07:15:20Z","timestamp":1600326920000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":74,"title":["Anti\u2010inflammatory treatment rescues memory deficits during aging in <i>nfkb1<\/i><sup>\u2212\/\u2212<\/sup> mice"],"prefix":"10.1111","volume":"19","author":[{"given":"Edward","family":"Fielder","sequence":"first","affiliation":[{"name":"Biosciences Institute Ageing Research Laboratories Campus for Ageing and Vitality Newcastle University Newcastle upon Tyne UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5627-3505","authenticated-orcid":false,"given":"Clare","family":"Tweedy","sequence":"additional","affiliation":[{"name":"Biosciences Institute Faculty of Medical Sciences Newcastle University Newcastle UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Caroline","family":"Wilson","sequence":"additional","affiliation":[{"name":"Bioscience Institute Immunity and Inflammation Newcastle Fibrosis Research Group Faculty of Medical Sciences Newcastle University Newcastle upon Tyne UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fiona","family":"Oakley","sequence":"additional","affiliation":[{"name":"Bioscience Institute Immunity and Inflammation Newcastle Fibrosis Research Group Faculty of Medical Sciences Newcastle University Newcastle upon Tyne UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fiona E. 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