These results on the one hand further reflect the vital role of Tau‐mediated NLRP3 acetylation and inflammasome activation in the phenotypes of microglia activation and cognitive dysfunction, and also indicate that targeting NLRP3 acetylation induced by Tau is a potential promising effective strategy for early AD and related Tauopathies therapy. This evidence concerns the gene NLRP3 and Alzheimer disease.