Peripheral clearance of amyloid β peptide by complement C3-dependent adherence to erythrocytes

被引：147

作者：

Rogers, Joseph

Li, Rena

Mastroeni, Diego

Grover, Andrew

Leonard, Brian

Ahern, Geoffrey

Cao, Phillip

Kolody, Heather

Vedders, Linda

Kolb, William P.

Sabbagh, Marwan

机构：

[1] LJ Roberts Ctr Alzheimers Res, Sun Hlth Res Inst, Sun City, AZ 85372 USA

[2] Univ Arizona, Coll Med, Dept Neurol, Tucson, AZ 85724 USA

[3] Adv Res Technol, San Diego, CA 92121 USA

来源：

NEUROBIOLOGY OF AGING | 2006年 / 27卷 / 12期

关键词：

amyloid beta peptide; complement; Alzheimer's disease; blood; clearance;

D O I：

10.1016/j.neurobiolaging.2005.09.043

中图分类号：

R592 [老年病学]; C [社会科学总论];

学科分类号：

03 [法学]; 0303 [社会学]; 100203 [老年医学];

摘要：

Brain deposits of amyloid (3 peptide (A(3) have been a diagnostic hallmark of Alzheimer's disease (AD) for nearly a century. Recent studies have demonstrated that A(3 is also present in peripheral blood. Here, we present evidence that circulating A(342 is subject to complement Cab-dependent adherence to complement receptor 1 (CR1) on erythrocytes, a classical set of mechanisms by which pathogens and proteins recognized as foreign are cleared from the bloodstream. Levels of A(342 targeted by this pathway differ significantly in AD compared to mild cognitive impairment and nondemented elderly controls. (c) 2005 Elsevier Inc. All rights reserved.

引用

页码：1733 / 1739

页数：7

共 24 条

[1]

[Anonymous], KIMBALLS BIOL PAGES

[2]

Peripherally administered antibodies against amyloid β-peptide enter the central nervous system and reduce pathology in a mouse model of Alzheimer disease [J].