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

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.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Webster S,Glabe C,Rogers J

doi

10.1006/bbrc.1995.2852

subject

Has Abstract

pub_date

1995-12-26 00:00:00

pages

869-75

issue

3

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(85)72852-5

journal_volume

217

pub_type

杂志文章

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