Amyloid‐β activates NLRP3 inflammasomes by affecting microglial immunometabolism through the Syk‐AMPK pathway

Neuroinflammation is considered one of major factors in the pathogenesis of Alzheimer’s disease (AD). In particular, inflammasome activation, including NLRP3 inflammasome in microglia, is regarded as fundamental for the pro‐inflammatory response of immune cells (Hanslik & Ulland, 2020). Aβ functions to primarily activate microglia in AD and reports have been made that Aβ can activate NLRP3 inflammasome(Halle et al., 2008). However, the precise molecular mechanism through which the NLRP3 inflammasome is associated with AD pathologies remains unclear.