NLRP3 inflammasome activation mediates tau pathology

Abstract summary

Showed that amyloid-beta activates the NLRP3 inflammasome in microglia, leading to caspase-1 activation and IL-1beta secretion. NLRP3-deficient mice have reduced amyloid burden and improved memory in AD mouse models. Identified NLRP3 as a critical microglial sensor of amyloid pathology.

Evidence labels

Therapeutic relevance

Established NLRP3 as a therapeutic target in AD; multiple NLRP3 inhibitors are in development for neurological indications.