NLRP3 inflammasome activation drives tau pathology.

ABSTRACT: Alzheimer's disease is characterized by the accumulation of amyloid-beta in plaques, aggregation of hyperphosphorylated tau in neurofibrillary tangles and neuroinflammation, together resulting in neurodegeneration and cognitive decline¹. The NLRP3 inflammasome assembles inside of microglia on activation, leading to increased cleavage and activity of caspase-1 and downstream interleukin-1β release². Although the NLRP3 inflammasome has been shown to be essential for the development and progression of amyloid-beta pathology in mice³, the precise effect on tau pathology remains unknown. Here we show that loss of NLRP3 inflammasome function reduced tau hyperphosphorylation and aggregation by regulating tau kinases and phosphatases. Tau activated the NLRP3 inflam

SUBMITTER: Ising C 

PROVIDER: S-EPMC7324015 | biostudies-literature | 2019 Nov

REPOSITORIES: biostudies-literature