Peripheral clearance of amyloid β peptide by complement C3-dependent adherence to erythrocytes
Document Type
Article
Abstract
Brain deposits of amyloid β peptide (Aβ) have been a diagnostic hallmark of Alzheimer's disease (AD) for nearly a century. Recent studies have demonstrated that Aβ is also present in peripheral blood. Here, we present evidence that circulating Aβ42 is subject to complement C3b-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 Aβ42 targeted by this pathway differ significantly in AD compared to mild cognitive impairment and nondemented elderly controls. © 2005 Elsevier Inc. All rights reserved.
Publication Date
12-1-2006
Publication Title
Neurobiology of Aging
ISSN
01974580
Volume
27
Issue
12
First Page
1733
Last Page
1739
PubMed ID
16290270
Digital Object Identifier (DOI)
10.1016/j.neurobiolaging.2005.09.043
Recommended Citation
Rogers, Joseph; Li, Rena; Mastroeni, Diego; Grover, Andrew; Leonard, Brian; Ahern, Geoffrey; Cao, Phillip; Kolody, Heather; Vedders, Linda; Kolb, William P.; and Sabbagh, Marwan, "Peripheral clearance of amyloid β peptide by complement C3-dependent adherence to erythrocytes" (2006). Neurology. 983.
https://scholar.barrowneuro.org/neurology/983