The NLRP3 inflammasome triggers sterile neuroinflammation and Alzheimer's disease

To maintain homeostasis, an organism must detect and resolve sterile tissue damage. The NLRP3 inflammasome coordinates such processes to clear tissue damage and induce repair. Dysregulated NLRP3 inflammasome activity, however, drives many conditions including Alzheimer's disease (AD). Recent reports posit that beta-amyloid and tau aggregates trigger destructive NLRP3 inflammasome signalling in the brain, leading to AD pathophysiology and cognitive decline. Other endogenous molecules (e.g. TNF, ATP, serum amyloid A), as well as dysbiosis, can induce peripheral or central inflammation and thereby promote microglial NLRP3 inflammasome signalling and resultant AD. The NLRP3 inflammasome is thus emerging as a critical driver of sterile neuroinflammation and the resultant pathogenesis and progression of AD.

Automated summary

Dysregulated activity of NLRP3 inflammasome can drive various conditions, including Alzheimer's disease. Recent studies suggest that beta-amyloid and tau aggregates may trigger destructive NLRP3 inflammasome signaling, leading to cognitive decline. Other endogenous molecules and dysbiosis can also induce inflammation and promote the development of Alzheimer's disease through microglial NLRP3 inflammasome signaling.