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Influence of lipoproteins on microglial degradation of Alzheimer's amyloid beta‐protein
Author(s) -
Cole Greg M.,
Ard March D.
Publication year - 2000
Publication title -
microscopy research and technique
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.536
H-Index - 118
eISSN - 1097-0029
pISSN - 1059-910X
DOI - 10.1002/1097-0029(20000815)50:4<316::aid-jemt11>3.0.co;2-e
Subject(s) - microglia , amyloid (mycology) , amyloid beta , beta (programming language) , chemistry , degradation (telecommunications) , biochemistry , neuroscience , biophysics , inflammation , biology , immunology , peptide , computer science , inorganic chemistry , telecommunications , programming language
Amyloid β‐protein (Aβ), the major component of plaques in Alzheimer's disease, is a small hydrophobic protein that is carried on apolipoprotein E (ApoE)‐ and ApoJ‐containing lipoprotein particles in plasma and cerebrospinal fluid (CSF). Microglia, the scavenger cells of the CNS, take up and degrade Aβ via lipoprotein receptors including scavenger receptors A and B, and possibly via other receptors. Lipoproteins, ApoE, and ApoJ influence the uptake and degradation of Aβ in vitro and in vivo. Differences in ApoE‐E4, ‐E3, and ‐E2 isoforms with respect to Aβ binding to lipoproteins and delivery to cells, including microglia, may contribute to the increased risk of Alzheimer's disease for people with an APOE 4 genotype and to risk reduction with APOE 2. Microsc. Res. Tech. 50:316–324, 2000. © 2000 Wiley‐Liss, Inc.