Premium
The role of innate immune responses and neuroinflammation in amyloid accumulation and progression of Alzheimer's disease
Author(s) -
Webers Alessandra,
Heneka Michael T,
Gleeson Paul A
Publication year - 2020
Publication title -
immunology and cell biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.999
H-Index - 104
eISSN - 1440-1711
pISSN - 0818-9641
DOI - 10.1111/imcb.12301
Subject(s) - neuroinflammation , microglia , inflammation , innate immune system , proinflammatory cytokine , neuroscience , immune system , amyloid (mycology) , neurodegeneration , alzheimer's disease , immunology , amyloid beta , biology , disease , medicine , pathology
Alzheimer's disease ( AD ) is characterized by amyloid beta (Aβ) accumulation, tau pathology and neuroinflammation. Recently, there has been considerable interest in the role of neuroinflammation in directly contributing to the progression of AD . Studies in mice and humans have identified a role for microglial cells, the resident innate immune cells of the central nervous system, in AD . Activated microglia are a key hallmark of the disease and the secretion of proinflammatory cytokines by microglia may result in a positive feedback loop between neurons and microglia, resulting in ongoing low‐grade inflammation. Traditionally, the pathways of Aβ production and neuroinflammation have been considered independently; however, recent studies suggest that these processes may converge to promote the pathology associated with AD . Here we review the importance of inflammation and microglia in AD development and effects of inflammatory responses on cellular pathways of neurons, including Aβ generation.