NLRP3 regulates microglial metabolic function in Alzheimer’s disease

Our laboratory has demonstrated that the NLRP3 inflammasome has a critical part in the microglial innate immune response to Alzheimer’s disease (AD)‐related peptides, triggering the production of cleaved‐caspase‐1 and IL‐1β. NLRP3 activation was found in post‐mortem tissue from individuals with AD (Heneka et al., 2013) and in transgenic mouse models of AD expressing amyloid precursor protein (APP) and presenilin 1 (PS1; APP/PS1 mice). However, APP/PS1 mice deficient for NLRP3 were protected from AD‐pathology and neuroinflammation. Here, we set out to determine the genes and pathways under the influence of NLRP3, beyond the established release of IL‐1β and ASC that could be contributing to the progression of AD.