In conclusion, although the precise roles of NLRP1 inflammasome activation in the development and progression of AD and other tauopathies have yet to be fully elucidated, our findings reveal region-specific mechanisms of NLRP1 inflammasome activation in the HF and suggest that its suppression represents a valid therapeutic goal for the treatment or prevention of AD. This evidence concerns the gene NLRP1 and Alzheimer disease.