The mouse C1q A-chain sequence alters beta-amyloid-induced complement activation

被引：38

作者：

Webster, SD

Tenner, AJ

Poulos, TL

Cribbs, DH ^{[1
]}

机构：

[1] Univ Calif Irvine, Dept Neurol, Inst Brain Aging & Dementia, Irvine, CA 92697 USA

[2] Univ Calif Irvine, Dept Biochem & Mol Biol, Irvine, CA 92697 USA

来源：

NEUROBIOLOGY OF AGING | 1999年 / 20卷 / 03期

关键词：

Alzheimer's disease; complement activation; C1q; neuroinflammation; neurodegeneration; beta-amyloid; transgenic;

D O I：

10.1016/S0197-4580(99)00020-2

中图分类号：

R592 [老年病学]; C [社会科学总论];

学科分类号：

03 ; 0303 ; 100203 ;

摘要：

In transgenic models of Alzheimer's disease (AD) neuronal loss has not been widely observed. The loss of neurons in AD may be due to chronic activation of complement (C') by beta-amyloid (A beta). A beta has been shown to activate C' by binding to a site on the Clq A-chain. The mouse A-chain sequence differs significantly from human, and a peptide based on the mouse A-chain sequence was ineffective at blocking activation of C' by A beta in contrast to the inhibition seen with the human peptide. Comparison of mouse and human serum showed that human C' was activated more effectively by A beta than was mouse C'. Therefore, additional genetic manipulations may be necessary to replicate in the murine model the inflammation and neurodegeneration that occur in AD. (C) 1999 Elsevier Science Inc. All rights reserved.

引用

页码：297 / 304

页数：8

共 45 条

[31] MOUSE STRAINS WITH TYPICAL MAMMALIAN LEVELS OF COMPLEMENT ACTIVITY [J].