title: Complement activation by beta-amyloid in Alzheimer disease.
abstract: 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.
authors.affiliation: L. J. Roberts Center, Sun Health Research Institute, Sun City, AZ 85351.
authors.forename: J
authors.initials: J
authors.lastname: Rogers
authors.forename: N R
authors.initials: NR
authors.lastname: Cooper
authors.forename: S
authors.initials: S
authors.lastname: Webster
authors.forename: J
authors.initials: J
authors.lastname: Schultz
authors.forename: P L
authors.initials: PL
authors.lastname: McGeer
authors.forename: S D
authors.initials: SD
authors.lastname: Styren
authors.forename: W H
authors.initials: WH
authors.lastname: Civin
authors.forename: L
authors.initials: L
authors.lastname: Brachova
authors.forename: B
authors.initials: B
authors.lastname: Bradt
authors.forename: P
authors.initials: P
authors.lastname: Ward
mesh_terms: 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
chemical_list: D016229:Amyloid beta-Peptides; D015922:Complement C1q