A recent pioneering study by Haneka et al. [73] showed that NLRP3 gene deletion in amyloid precursor protein (APP)/presenilin 1 (PS1) mice (animal model of AD) attenuated learning and memory deficits, neocortex neuronal loss and brain Aβ accumulation, by increasing Aβ phagocytic clearance capacity and insulin-degrading enzyme (IDE) expression (an enzyme able to degrade extracellular Aβ). Here, NLRP3 is linked to Alzheimer disease.