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Summary   Background  Activated microglia‐mediated inflammation plays a key role in the pathogenesis of Alzheimer’s disease ( AD ). In addition, chronic activation of  NLRP 3 inflammasomes triggered by amyloid β peptide (Aβ) in microglia contributes to persistent neuroinflammation. Here, the primary goal was to assess whether Dihydromyricetin ( DHM ), a plant flavonoid compound, is effective therapies for  AD ; it is crucial to know whether  DHM  will affect microglial activation and neuroinflammation in  APP / PS 1 transgenic mice.    Methods  After  DHM  was intraperitoneally injected in  APP / PS 1 double‐transgenic mice, we assessed the effect of  DHM  on microglial activation, the expression of  NLRP 3 inflammasome components, and the production of inflammatory cytokine  IL ‐1β by immunofluorescence and Western blot. To determine whether  DHM  play roles in the Aβ production and deposition, amyloid β protein precursor ( APP ) and β‐site  APP  cleaving enzyme1 ( BACE 1), as well as neprilysin ( NEP ), were detected by Western blot. Finally, behavior was tested by Morris Water Maze to illustrate whether  DHM  treatment has a significantly positive effect on ameliorating the memory and cognition deficits in  AD .    Results  Dihydromyricetin treatment significantly ameliorated memory and cognition deficits and decreased the number of activated microglia in the hippocampus and cortex of  APP / PS 1 mice. In addition,  APP / PS 1 mice show reduced activation of  NLRP 3 inflammasomes and reduced expression of  NLRP 3 inflammasome components. Furthermore,  DHM  could promote clearance of Aβ, a trigger for  NLRP 3 inflammasome activation, by increasing levels of  NEP  and shift microglial conversion to the M2‐specific agrinase‐1‐positive cell phenotype, which enhances microglial clearance of Aβ and its aggregates but not production of Aβ.    Conclusion  Taken together, our findings suggest that  DHM  prevents progression of  AD ‐like pathology through inhibition of  NLRP 3 inflammasome‐based microglia‐mediated neuroinflammation and may be a promising therapeutic drug for treating  AD .

Dihydromyricetin inhibits microglial activation and neuroinflammation by suppressing NLRP 3 inflammasome activation in APP / PS 1 transgenic mice