Involvement of Microglial Receptor for Advanced Glycation Endproducts (RAGE) in Alzheimer's Disease: Identification of a Cellular Activation Mechanism

Lue, Lih-Fen; Walker, Douglas G.; Brachova, Libuse; Beach, Thomas G.; Rogers, Joseph; Schmidt, Ann Marie; Stern, David M.; Yan, Shi Du

doi:10.1006/exnr.2001.7732

Cited by 439Advanced Glycation End Products researchNeuroinflammation and Neurodegeneration MechanismsAlzheimer's disease research and treatments

Involvement of Microglial Receptor for Advanced Glycation Endproducts (RAGE) in Alzheimer's Disease: Identification of a Cellular Activation Mechanism

Lue, Lih-Fen, Walker, Douglas G., Brachova, Libuse, Beach, Thomas G., Rogers, Joseph, Schmidt, Ann Marie, Stern, David M., Yan, Shi Du·2001·Experimental Neurology

DOI 10.1006/exnr.2001.7732

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Abstract

Receptor-mediated interactions with amyloid beta-peptide (Abeta) could be important in the evolution of the inflammatory processes and cellular dysfunction that are prominent in Alzheimer's disease (AD) pathology. One candidate receptor is the receptor for advanced glycation endproducts (RAGE), which can bind Abeta and transduce signals leading to cellular activation. Data are presented showing a potential mechanism for Abeta activation of microglia that could be mediated by RAGE and macrophage colony-stimulating factor (M-CSF). Using brain tissue from AD and nondemented (ND) individuals, RAGE expression was shown to be present on microglia and neurons of the hippocampus, entorhinal cortex, and superior frontal gyrus. The presence of increased numbers of RAGE-immunoreactive microglia in AD led us to further analyze RAGE-related properties of these cells cultured from AD and ND brains. Direct addition of Abeta(1-42) to the microglia increased their expression of M-CSF. This effect was significantly greater in microglia derived from AD brains compared to those from ND brains. Increased M-CSF secretion was also demonstrated using a cell culture model of plaques whereby microglia were cultured in wells containing focal deposits of immobilized Abeta(1-42). In each case, the Abeta stimulation of M-CSF secretion was significantly blocked by treatment of cultures with anti-RAGE F(ab')2. Treatment of microglia with anti-RAGE F(ab')2 also inhibited the chemotactic response of microglia toward Abeta(1-42). Finally, incubation of microglia with M-CSF and Abeta increased expression of RAGE mRNA. These microglia also expressed M-CSF receptor mRNA. These data suggest a positive feedback loop in which Abeta-RAGE-mediated microglial activation enhances expression of M-CSF and RAGE, possibly initiating an ascending spiral of cellular activation.

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Five papers identified no difference in major histocompatibility complex II in at least one brain region.
“and 5 identified no difference in at least one brain region.21, 32, 34, 41, 44”
From Markers of microglia in post-mortem brain samples from patients with Alzheimer’s disease: a systematic review (2018) · cites this paper as [34]
Of five studies examining HLA-DR immunoreactivity in the cerebellum, four found no differences between Alzheimer's disease and control.
“Of the five studies examining HLA-DR immunoreactivity in the cerebellum, four found no differences between AD and control,25, 34, 44, 51”
From Markers of microglia in post-mortem brain samples from patients with Alzheimer’s disease: a systematic review (2018) · cites this paper as [34]
More than half the studies that used tissue from the cerebellum identified no difference between control and AD across a range of microglial markers.
“More than half the studies that used tissue from the cerebellum identified no difference between control and AD across a range of microglial markers.25, 34, 44, 112, 178”
From Markers of microglia in post-mortem brain samples from patients with Alzheimer’s disease: a systematic review (2018) · cites this paper as [34]
RAGE is elevated in AD brain vasculature and activated microglia.
“To enhance brain enrichment, we exploited the elevated expression of RAGE in AD brain vasculature and activated microglia [ 15, 46, 47 ].”
From Restores Aβ Clearance by Overcoming PCSK9–LRP1 Dysregulation and TRIB3‐Mediated Autophagy Blockade in Alzheimer's Disease (2026) · cites this paper as [47]
In AD patient brain, RAGE binding to Aβ promotes microglia migration to amyloid plaques and NF-κB activation, leading to neuroinflammatory activation.
“In AD patient brain, RAGE binding to Aβ can promote microglia migration to amyloid plaques and NF-κB activation, consequently leading to neuroinflammatory activation [367].”
From Molecular and cellular mechanisms underlying the pathogenesis of Alzheimer’s disease (2020) · cites this paper as [367]

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Authors: Lue, L.-F., Walker, D. G., Brachova, L., Beach, T. G., Rogers, J., Schmidt, A. M., Stern, D. M., & Yan, S. D.
Affiliations: Banner Sun Health Research Institute (US)
Columbia University (US)
Corresponding author: Lue, Lih-Fen
ORCID: Lue, Lih-Fen
Walker, Douglas G.
Venue: Experimental Neurology
Publisher: Elsevier BV
Published: 2001-09
Volume: 171
Issue: 1
Pages: 29-45
ISSN: 0014-4886 (ISSN-L)
DOI: 10.1006/exnr.2001.7732
OpenAlex: W2003813921
Cited by: 439
References: 73
Citations by year: 2026: 10 · 2025: 14 · 2024: 9 · 2023: 19 · 2022: 19 · 2021: 31 · 2020: 20 · 2019: 14 · 2018: 17 · 2017: 14 · 2016: 16 · 2015: 28 · 2014: 24 · 2013: 17 · 2012: 27
FWCI: 6.92
Type: journal article
Language: en
Open access: closed
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
www.elsevier.com/legal/tdmrep-license (tdm)
Locations: Experimental Neurology (publishedVersion)
PubMed (publishedVersion)
Funders: National Institutes of Health (HL60901, AG00690, AG14103, AG07367, HL56881, AG16736)
Burroughs Wellcome Fund
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Clinical Biochemistry › Advanced Glycation End Products research
Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
Keywords: Alzheimer's disease, receptor for advanced glycation end products, RAGE, amyloid-beta, microglial activation, macrophage colony-stimulating factor, M-CSF receptor, neuroinflammation, amyloid plaques, chemotaxis, hippocampus, entorhinal cortex, superior frontal gyrus
MeSH terms: Receptor for Advanced Glycation End Products, Aged, Aged, 80 and over, Alzheimer Disease, Cells, Cultured, Chemotaxis, Dose-Response Relationship, Drug, Feedback, Female, Frontal Lobe, Hippocampus, Humans, Immunoglobulin Fab Fragments, Immunohistochemistry, Male, Middle Aged, Neurons, Peptide Fragments, Receptors, Immunologic, RNA, Messenger, Signal Transduction, Macrophage Colony-Stimulating Factor, Amyloid beta-Peptides, Microglia, Entorhinal Cortex

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Involvement of Microglial Receptor for Advanced Glycation Endproducts (RAGE) in Alzheimer's Disease: Identification of a Cellular Activation Mechanism

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