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Neural cell injury contributes to the neurological deficits observed in CM. Abnormal regulation of tau, an axonal protein pathologically associated with the formation of neurofibrillary lesions in neurodegenerative diseases, has been linked to inflammation and cerebral microvascular compromise and has been reported in human and experimental CM (ECM). Immunotherapy with a monoclonal antibody to pathological tau (PHF\u20101 mAB) in experimental models of neurodegenerative diseases has been reported to mitigate cognitive decline. We investigated whether immunotherapy with PHF\u20101 mAB prevented cerebral endotheliopathy, neural cell injury, and neuroinflammation during ECM. Using C57BL\/6 mice infected with either <jats:italic>Plasmodium berghei<\/jats:italic> ANKA (PbA), which causes ECM, <jats:italic>Plasmodium berghei<\/jats:italic> NK65 (PbN), which causes severe malaria, but not ECM, or uninfected mice (Un), we demonstrated that when compared to PbN infection or uninfected mice, PbA infection resulted in significant memory impairment at 6\u2009days post\u2010infection, in association with abnormal tau phosphorylation at Ser<jats:sup>202<\/jats:sup>\/Thr<jats:sup>205<\/jats:sup> (pSer<jats:sup>202<\/jats:sup>\/Thr<jats:sup>205<\/jats:sup>) and Ser<jats:sup>396\u2013404<\/jats:sup> (pSer<jats:sup>396\u2013404<\/jats:sup>) in mouse brains. ECM also resulted in significantly higher expression of inflammatory markers, in microvascular congestion, and glial cell activation. Treatment with PHF\u20101 mAB prevented PbA\u2010induced cognitive impairment and was associated with significantly less vascular congestion, neuroinflammation, and neural cell activation in mice with ECM. These findings suggest that abnormal regulation of tau protein contributes to cerebral vasculopathy and is critical in the pathogenesis of neural cell injury during CM. Tau\u2010targeted therapies may ameliorate the neural cell damage and subsequent neurocognitive impairment that occur during disease.<jats:boxed-text content-type=\"graphic\" position=\"anchor\"><jats:graphic xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" mimetype=\"image\/png\" position=\"anchor\" specific-use=\"enlarged-web-image\" xlink:href=\"graphic\/jnc15972-fig-0010-m.png\"><jats:alt-text>image<\/jats:alt-text><\/jats:graphic><\/jats:boxed-text><\/jats:p>","DOI":"10.1111\/jnc.15972","type":"journal-article","created":{"date-parts":[[2023,10,12]],"date-time":"2023-10-12T02:42:14Z","timestamp":1697078534000},"page":"441-460","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":7,"title":["Effects of anti\u2010tau immunotherapy on reactive microgliosis, cerebral endotheliopathy, and cognitive function in an experimental model of cerebral 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