This result was confirmed by Heneka and colleagues, who showed that NLRP3-deficiency in the transgenic APP/PS1 double-transgenic mouse models of AD, which overexpressed mutated forms of the gene for human amyloid precursor protein (APP) and presenilin 1 (PS1), decreased neuroinflammation, reducing Aβ accumulation and improving neuronal function [21]. Here, APP is linked to Alzheimer disease.