炎症体
神经炎症
炎症
小胶质细胞
内生
神经科学
发病机制
生物
免疫学
细胞生物学
生物化学
作者
Mark Thomas Milner,Madhavi P. Maddugoda,Jürgen Götz,Sabrina Sofia Burgener,Kate Schroder
标识
DOI:10.1016/j.coi.2020.10.011
摘要
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 β-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.
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