NLRP3 inflammasome activation drives tau pathology

Loss of NLRP3 inflammasome function reduced tau hyperphosphorylation and aggregation.

• The NLRP3 inflammasome is activated in microglia, leading to increased activity of caspase-1 and release of interleukin-1β.
• In mice, the NLRP3 inflammasome is essential for the development of amyloid-beta pathology.
• Tau can activate the NLRP3 inflammasome, linking tau pathology to amyloid-beta-induced microglial activation.
• Intracerebral injection of amyloid-beta-containing brain homogenates induced tau pathology in an NLRP3-dependent manner.
• The findings suggest that microglial activation and NLRP3 inflammasome play significant roles in the development of tauopathies.

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