BETA-AMYLOID PEPTIDES INITIATE THE COMPLEMENT CASCADE WITHOUT PRODUCING A COMPARABLE EFFECT ON THE TERMINAL PATHWAY IN-VITRO

Activation of the classical complement cascade by beta-amyloid peptide s has been hypothesized to underlie the neurodegeneration observed in Alzheimer's diseased brains. In this study, various lots of synthetic beta-amyloid peptides, A beta(1-40), A beta(1-42), and A beta(25-35), were tested for their ability to activate both early complement cascad e events and formation of the membrane attack complex through terminal pathway activation. Unlike recent reports which did not assess activa tion of complement terminal pathway, we found that concentrations of b eta-amyloid which activated early cascade events, to an extent compara ble to aggregated IgG, failed to elicit formation of comparable levels of membrane attack complex. (C) 1997 Academic Press.