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Alzheimer\u2019s disease (AD), the most common neurodegenerative disorder, is characterized by the accumulation of amyloid-<jats:italic>\u03b2<\/jats:italic> (A<jats:italic>\u03b2<\/jats:italic>) peptide and hyperphosphorylated tau protein. Accumulating evidence has revealed that the slow progressive deterioration of AD is associated with oxidative stress and chronic inflammation in the brain. Nuclear factor erythroid 2- (NF-E2-) related factor 2 (Nrf2), which acts through the Nrf2\/ARE pathway, is a key regulator of the antioxidant and anti-inflammatory response. Although recent data show a link between Nrf2 and AD-related cognitive decline, the mechanism is still unknown. Thus, we explored how Nrf2 protects brain cells against the oxidative stress and inflammation of AD in a mouse model of AD (APP\/PS1 transgenic (AT) mice) with genetic removal of Nrf2. <jats:italic>Methods<\/jats:italic>. The spatial learning and memory abilities of 12-month-old transgenic mice were evaluated using a Morris water maze test. Hippocampal levels of Nrf2, A<jats:italic>\u03b2<\/jats:italic>, and p-tauS404 and of astrocytes and microglia were determined by immunostaining. Inflammatory cytokines were determined by ELISA and quantitative real-time polymerase chain reaction (qRT-PCR). Oxidative stress was measured by 8-hydroxydeoxyguanosine immunohistochemistry, and the antioxidant response was determined by qRT-PCR. <jats:italic>Results<\/jats:italic>. The spatial learning and memory abilities of AT mice were impaired after Nrf2 deletion. A<jats:italic>\u03b2<\/jats:italic> and p-tauS404 accumulation was increased in the hippocampus of AT\/Nrf2-KO mice. Astroglial and microglial activation was exacerbated, followed by upregulation of the proinflammatory cytokines IL-1<jats:italic>\u03b2<\/jats:italic>, IL-6, and TNF-<jats:italic>\u03b1<\/jats:italic>. <jats:italic>Conclusion<\/jats:italic>. Our present results show that Nrf2 deficiency aggravates AD-like pathology in AT mice. This phenotype was associated with increased levels of oxidative and proinflammatory markers, which suggests that the Nrf2 pathway may be a promising therapeutic target for AD.<\/jats:p>","DOI":"10.1155\/2020\/3050971","type":"journal-article","created":{"date-parts":[[2020,5,11]],"date-time":"2020-05-11T23:41:32Z","timestamp":1589240492000},"page":"1-13","source":"Crossref","is-referenced-by-count":91,"title":["Nrf2 Ablation Promotes Alzheimer\u2019s Disease-Like Pathology in APP\/PS1 Transgenic Mice: The Role of Neuroinflammation and Oxidative Stress"],"prefix":"10.1155","volume":"2020","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-4282-5839","authenticated-orcid":true,"given":"Peng","family":"Ren","sequence":"first","affiliation":[{"name":"Department of Forensic Pathology, School of Forensic Medicine, China Medical University, Shenyang, Liaoning 110122, China"},{"name":"Department of Forensic Medicine, Criminal Investigation Police University of China, Shenyang, Liaoning 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