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Senescent cells accumulate in the aging brain, accelerate the aging process, and promote tauopathy progression through their abnormal inflammatory secretome known as the senescence\u2010associated secretory phenotype (SASP). Tau oligomers (TauO)\u2014the most neurotoxic tau species\u2014are known to induce senescence and the SASP, which subsequently promote neuropathology, inflammation, oxidative stress, synaptic dysfunction, neuronal death, and cognitive dysfunction. TauO, brain inflammation, and senescence are associated with heterogeneity in tauopathy progression and cognitive decline. However, the underlying mechanisms driving the disease heterogeneity remain largely unknown, impeding the development of therapies for tauopathies. Based on clinical and preclinical evidence, this review highlights the critical role of TauO and senescence in neurodegeneration. We discuss key knowledge gaps and potential strategies for targeting senescence and TauO to treat tauopathies.<\/jats:p><\/jats:sec><jats:sec><jats:title>Highlights<\/jats:title><jats:p><jats:list list-type=\"bullet\">\n<jats:list-item><jats:p>Senescence, oligomeric Tau (TauO), and brain inflammation accelerate the aging process and promote the progression of tauopathies, including Alzheimer's disease.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>We discuss their role in contributing to heterogeneity in tauopathy and cognitive decline.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>We highlight strategies to target senescence and TauO to treat tauopathies while addressing key knowledge gaps.<\/jats:p><\/jats:list-item>\n<\/jats:list><\/jats:p><\/jats:sec>","DOI":"10.1002\/alz.13490","type":"journal-article","created":{"date-parts":[[2023,10,11]],"date-time":"2023-10-11T22:55:38Z","timestamp":1697064938000},"page":"709-727","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":117,"title":["Senescence, brain inflammation, and oligomeric tau drive cognitive decline in Alzheimer's disease: Evidence from clinical and preclinical studies"],"prefix":"10.1002","volume":"20","author":[{"given":"Sagar","family":"Gaikwad","sequence":"first","affiliation":[{"name":"The Mitchell Center for Neurodegenerative Diseases and Department of Neurology University of Texas Medical Branch  Galveston Texas USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sudipta","family":"Senapati","sequence":"additional","affiliation":[{"name":"The Mitchell Center for Neurodegenerative Diseases and Department of Neurology University of Texas Medical Branch  Galveston Texas USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Md. 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