Additionally, Asc−/− and Nlrp3−/− mice were resistant to tau hyperphosphorylation in the Tau22 model after injection of Aβ-containing brain homogenates [63], implying that the NLRP3 inflammasome is a potential therapeutic target for inhibiting both amyloid deposition and tau tangle formation during AD. Here, NLRP3 is linked to Alzheimer disease.