Abstract
Microglia are immune system cells associated with Alzheimer's disease plaques containing beta-amyloid (A beta). Murine microglia internalize microaggregates of fluorescently labeled or radioiodinated A beta peptide 1-42. Uptake was confirmed using aggregates of unlabeled A beta detected by immunofluorescence. Uptake of A beta was reduced by coincubation with excess acetyl-low density lipoprotein (Ac-LDL) or other scavenger receptor (SR) ligands, and Dil-labeled Ac-LDL uptake by microglia was blocked by excess A beta. CHO cells transfected with class A or B SRs showed significantly enhanced uptake of A beta. These results show that microglia express SRs that may play a significant role in the clearance of A beta plaques. Binding to SRs could activate inflammation responses that contribute to the pathology of Alzheimer's disease.
Publication types
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Alzheimer Disease / metabolism*
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Amyloid beta-Peptides / metabolism*
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Amyloid beta-Protein Precursor / genetics
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Animals
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Antineoplastic Agents / pharmacology
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Biological Transport / physiology
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Brain Chemistry / physiology
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Carbocyanines
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Cholesterol, LDL / pharmacology
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Fluorescent Dyes
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Intracellular Membranes / physiology
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Kinetics
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Lipoproteins / pharmacology
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Mice
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Microglia / chemistry*
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Microglia / physiology*
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Mutation
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Polysaccharides / pharmacology
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Receptors, Cell Surface / antagonists & inhibitors
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Receptors, Cell Surface / physiology*
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alpha-Macroglobulins / metabolism
Substances
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Amyloid beta-Peptides
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Amyloid beta-Protein Precursor
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Antineoplastic Agents
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Carbocyanines
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Cholesterol, LDL
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Fluorescent Dyes
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Lipoproteins
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Polysaccharides
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Receptors, Cell Surface
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alpha-Macroglobulins
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didodecylindocarbocyanine
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fucoidan