Proceedings of the National Academy of Sciences · 1992 · 814 citations · 24 references
Life SciencesNeurobiologyNeuroscienceNeurodegenerationNeuroimmunologyNeurotoxicologyAlzheimer DiseaseComplement SystemComplement-mediated InjuryNeurodegenerative DiseasesNeurodegenerative DisordersNeuroinflammationAlzheimer Disease NeuroimmunologyAmyloid Beta PeptidesAmyloid Beta PlaquesAmyloid-beta-induced NeurotoxicityComplement Activation PathwaysComplement In Disease PathogenesisComplement In Neurodegenerative DiseaseComplement In Neuroinflammation
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.
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The precursor of Alzheimer's disease amyloid A4 protein resembles a cell-surface receptor
Jie Kang, Hans-Georg Lemaire, Axel Unterbeck et al. · Nature · 1987 · 4.6K citations