In fact, while Aβ accumulated in the brain of APP/PS1 mice and triggered AD symptoms, impairment of the Nlrp3 gene in these mice ameliorated their AD phenotype: APP/PS1/Nlrp3-/- mice have decreased IL-1β levels in total brain, absence of caspase-1 cleavage and improved memory test. This evidence concerns the gene CASP1 and Alzheimer disease.