Figure 9. A functional model of KA-induced inflammasome activity through tau phosphorylation and memory deficits were exacerbated in an ER stress-dependent mechanism. KA treatment triggers activation of the inflammasome and causes the phosphorylation of NF-κB, leading to NLRP3 upregulation via ER stress. Upregulated NLRP3 eventually results in the phosphorylation of tau by enhancing the expression of IL-1β. Bay11-7082 inhibits KA-induced IL-1β activation and tau phosphorylation by alleviating the activity of inflammasome, which ultimately improved the cognitive decline in MAPT Tg mice.