Complement activation by beta-amyloid in Alzheimer disease.
Alzheimer disease (AD) is characterized by excessive deposition of the beta-amyloid peptide (beta-AP) in the central nervous system. Although several lines of evidence suggest that beta-AP is neurotoxic, a mechanism for beta-AP toxicity in AD brain remains unclear. In this paper we provide both direct in vitro evidence that beta-AP can bind and activate the classical complement cytolytic pathway in the absence of antibody and indirect in situ evidence that such actions occur in the AD brain in association with areas of AD pathology.
Rogers
J
J
L. J. Roberts Center, Sun Health Research Institute, Sun City, AZ 85351.
Cooper
N R
NR
Webster
S
S
Schultz
J
J
McGeer
P L
PL
Styren
S D
SD
Civin
W H
WH
Brachova
L
L
Bradt
B
B
Ward
P
P
D000544:Alzheimer Disease / Q000276:immunology* / Q000473:pathology; D016229:Amyloid beta-Peptides / Q000502:physiology*; D001921:Brain / Q000473:pathology / Q000503:physiopathology*; D003167:Complement Activation; D015922:Complement C1q / Q000032:analysis / Q000378:metabolism; D003171:Complement Pathway, Classical; D004797:Enzyme-Linked Immunosorbent Assay; D006801:Humans; D009928:Organ Specificity
D016229:Amyloid beta-Peptides; D015922:Complement C1q