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 peptides 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 cascade events and formation of the membrane attack complex through terminal pathway activation. Unlike recent reports which did not assess activation of complement terminal pathway, we found that concentrations of beta-amyloid which activated early cascade events, to an extent comparable to aggregated IgG, failed to elicit formation of comparable levels of membrane attack complex.