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Biochem Biophys Res Commun. 1995 Dec 26;217(3):869-75.

Multivalent binding of complement protein C1Q to the amyloid beta-peptide (A beta) promotes the nucleation phase of A beta aggregation.

Author information

1
L.J. Roberts Center for Alzheimer's Research, Sun Health Research Institute, Sun City, AZ 85372, USA.

Abstract

Activation of the classical complement pathway has been proposed as a mechanism of neurodegeneration in Alzheimer's disease. This activation is a result of the binding of C1q to amyloid beta-peptide (A beta). Recent work has shown that A beta/C1q binding has an additional consequence: enhanced formation of the neurotoxic, fibrillar, cross beta-pleated A beta configuration. Here we show that C1q enhances A beta aggregation at physiologically relevant, nanomolar concentrations of the peptides, and demonstrate that the kinetics of this enhancement are consistent with a nucleating interaction. We also show that the intact, multimeric structure of C1q, which offers multiple A beta binding sites spaced at 2-3 nm intervals, is required.

PMID:
8554610
DOI:
10.1006/bbrc.1995.2852
[Indexed for MEDLINE]

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