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In addition, chronic activation of NLRP<\/jats:styled-content>3 inflammasomes triggered by amyloid \u03b2 peptide (A\u03b2) in microglia contributes to persistent neuroinflammation. Here, the primary goal was to assess whether Dihydromyricetin (DHM<\/jats:styled-content>), a plant flavonoid compound, is effective therapies for AD<\/jats:styled-content>; it is crucial to know whether DHM<\/jats:styled-content> will affect microglial activation and neuroinflammation in APP<\/jats:styled-content>\/PS<\/jats:styled-content>1 transgenic mice.<\/jats:p><\/jats:sec>Methods<\/jats:title>After DHM<\/jats:styled-content> was intraperitoneally injected in APP<\/jats:styled-content>\/PS<\/jats:styled-content>1 double\u2010transgenic mice, we assessed the effect of DHM<\/jats:styled-content> on microglial activation, the expression of NLRP<\/jats:styled-content>3 inflammasome components, and the production of inflammatory cytokine IL<\/jats:styled-content>\u20101\u03b2 by immunofluorescence and Western blot. To determine whether DHM<\/jats:styled-content> play roles in the A\u03b2 production and deposition, amyloid \u03b2 protein precursor (APP<\/jats:styled-content>) and \u03b2\u2010site APP<\/jats:styled-content> cleaving enzyme1 (BACE<\/jats:styled-content>1), as well as neprilysin (NEP<\/jats:styled-content>), were detected by Western blot. Finally, behavior was tested by Morris Water Maze to illustrate whether DHM<\/jats:styled-content> treatment has a significantly positive effect on ameliorating the memory and cognition deficits in AD<\/jats:styled-content>.<\/jats:p><\/jats:sec>Results<\/jats:title>Dihydromyricetin treatment significantly ameliorated memory and cognition deficits and decreased the number of activated microglia in the hippocampus and cortex of APP<\/jats:styled-content>\/PS<\/jats:styled-content>1 mice. In addition, APP<\/jats:styled-content>\/PS<\/jats:styled-content>1 mice show reduced activation of NLRP<\/jats:styled-content>3 inflammasomes and reduced expression of NLRP<\/jats:styled-content>3 inflammasome components. Furthermore, DHM<\/jats:styled-content> could promote clearance of A\u03b2, a trigger for NLRP<\/jats:styled-content>3 inflammasome activation, by increasing levels of NEP<\/jats:styled-content> and shift microglial conversion to the M2\u2010specific agrinase\u20101\u2010positive cell phenotype, which enhances microglial clearance of A\u03b2 and its aggregates but not production of A\u03b2.<\/jats:p><\/jats:sec>Conclusion<\/jats:title>Taken together, our findings suggest that DHM<\/jats:styled-content> prevents progression of AD<\/jats:styled-content>\u2010like pathology through inhibition of NLRP<\/jats:styled-content>3 inflammasome\u2010based microglia\u2010mediated neuroinflammation and may be a promising therapeutic drug for treating AD<\/jats:styled-content>.<\/jats:p><\/jats:sec>","DOI":"10.1111\/cns.12983","type":"journal-article","created":{"date-parts":[[2018,6,5]],"date-time":"2018-06-05T04:40:51Z","timestamp":1528173651000},"page":"1207-1218","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":104,"title":["Dihydromyricetin inhibits microglial activation and neuroinflammation by suppressing NLRP<\/scp>3 inflammasome activation in APP<\/scp>\/PS<\/scp>1 transgenic mice"],"prefix":"10.1111","volume":"24","author":[{"given":"Jie","family":"Feng","sequence":"first","affiliation":[{"name":"Institute of Neuroscience Chongqing Medical University Chongqing China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jing\u2010Xue","family":"Wang","sequence":"additional","affiliation":[{"name":"Institute of Immunology Third Military Medical University Chongqing 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