Whether, when and how chronic inflammation increases the risk of developing late-onset Alzheimer's disease.

ABSTRACT: Neuropathological studies have revealed the presence of a broad variety of inflammation-related proteins (complement factors, acute-phase proteins, pro-inflammatory cytokines) in Alzheimer's disease (AD) brains. These constituents of innate immunity are involved in several crucial pathogenic events of the underlying pathological cascade in AD, and recent studies have shown that innate immunity is involved in the etiology of late-onset AD. Genome-wide association studies have demonstrated gene loci that are linked to the complement system. Neuropathological and experimental studies indicate that fibrillar amyloid-β (Aβ) can activate the innate immunity-related CD14 and Toll-like receptor signaling pathways of glial cells for pro-inflammatory cytokine production. The production capacity of t

SUBMITTER: Eikelenboom P 

PROVIDER: S-EPMC3506930 | biostudies-literature | 2012 Jun

REPOSITORIES: biostudies-literature