Complement activation as a biomarker for Alzheimer's disease

被引：51

作者：

Aiyaz, Mohammed ^{[1
]}

Lupton, Michelle K. ^{[1
]}

Proitsi, Petroula ^{[1
]}

Powell, John F. ^{[1
]}

Lovestone, Simon ^{[1
]}

机构：

[1] Kings Coll London, Inst Psychiat, London SE5 8AF, England

来源：

IMMUNOBIOLOGY | 2012年 / 217卷 / 02期

关键词：

Alzheimer's disease; Biomarker; Blood; Complement; Genetic risk factors; Inflammation; Plasma; C-REACTIVE PROTEIN; FACTOR-H POLYMORPHISM; GENOME-WIDE ASSOCIATION; AGE-RELATED MACULOPATHY; CEREBROSPINAL-FLUID; MACULAR DEGENERATION; APOLIPOPROTEIN-E; RECEPTOR; PLASMA BIOMARKERS; ALPHA; 1-ANTICHYMOTRYPSIN;

D O I：

10.1016/j.imbio.2011.07.023

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

There is increasing evidence from genetic, immunohistochemical, proteomic and epidemiological studies as well as in model systems that complement activation has an important role in the pathogenesis of Alzheimer's disease (AD). The complement cascade is an essential element of the innate immune response. In the brain complement proteins are integral components of amyloid plaques and complement activation occurs at the earliest stage of the disease. The complement cascade has been implicated as a protective mechanism in the clearance of amyloid, and in a causal role through chronic activation of the inflammatory response. In this review we discuss the potential for complement activation to act as a biomarker for AD at several stages in the disease process. An accurate biomarker that has sufficient predictive, diagnostic and prognostic value would provide a significant opportunity to develop and test for effective novel therapies in the treatment of AD. (C) 2011 Elsevier GmbH. All rights reserved.

引用

页码：204 / 215

页数：12

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