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RAGE‐dependent signaling in microglia contributes to neuroinflammation, Aβ accumulation, and impaired learning/memory in a mouse model of Alzheimer's disease
Open accessAbstract
Microglia are critical for amyloid‐β peptide (Aβ)‐mediated neuronal perturbation relevant to Alzheimer's disease (AD) pathogenesis. We demonstrate that overexpression of receptor for advanced glycation end products (RAGE) in imbroglio exaggerates neuroinflammation, as evidenced by increased proinflammatory mediator production, Aβ accumulation, impaired learning/memory, and neurotoxicity in an Aβ‐rich environment. Transgenic (Tg) mice expressing human mutant APP (mAPP) in neurons and RAGE in microglia displayed enhanced IL‐1β and TNF‐α production, increased infiltration of microglia and astrocytes, accumulation of Aβ, reduced acetylcholine esterase (AChE) activity, and accelerated deterioration of spatial learning/memory. Notably, introduction of a signal transduction‐defective mutant RAGE (DN‐RAGE) to microglia attenuates deterioration induced by Aβ. These findings indicate that RAGE signaling in microglia contributes to the pathogenesis of an inflammatory response that ultimately impairs neuronal function and directly affects amyloid accumulation. We conclude that blockade of microglial RAGE may have a beneficial effect on Aβ‐mediated neuronal perturbation relevant to AD pathogenesis.—Fang, F., Lue, L.‐F., Yan, S., Xu, H., Luddy, J. S., Chen, D., Walker, D. G., Stern, D. M., Yan, S., Schmidt, A. M., Chen, J. X., Yan, S. S. RAGE‐dependent signaling in microglia contributes to neuroinflammation, Aβ accumulation, and impaired learning/memory in a mouse model of Alzheimer's disease. FASEB J. 24, 1043–1055 (2010). www.fasebj.org
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“In APP transgenic mice, overexpression of RAGE in microglia increases glial infiltration and Aβ accumulation, and exacerbates cognitive function [375].”
From Molecular and cellular mechanisms underlying the pathogenesis of Alzheimer’s disease (2020) · cites this paper as [375]
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“In addition, the binding of β-amyloid to RAGe results in activated microglial cells94, and RAGe expression by microglial cells contributed to neuroinflammation in a mouse model of Alzheimer's disease89.”
From Sterile inflammation: sensing and reacting to damage (2010) · cites this paper as [89]
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“RAGe is a transmembrane receptor that is expressed by immune cells, endothelial cells, cardiomyocytes and neurons89–91.”
From Sterile inflammation: sensing and reacting to damage (2010) · cites this paper as [89]
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Metadata
- Authors
- Fang, F., Lue, L.-F., Yan, S., Xu, H., Luddy, J. S., Chen, D., Walker, D. G., Stern, D. M., Yan, S., Schmidt, A. M., Chen, J. X., & Yan, S. S.
- Affiliations
- Columbia University Irving Medical Center (US)
- Banner Sun Health Research Institute (US)
- Harbin Medical University (CN)
- University of Cincinnati (US)
- Department of Surgery College of Physicians and Surgeons Columbia University New York New York USA
- Memorial Sloan Kettering Cancer Center (US)
- Corresponding author
- Yan, Shirley ShiDu
- Venue
- The FASEB Journal
- Publisher
- Wiley
- Published
- 2009-11-11
- Volume
- 24
- Issue
- 4
- Pages
- 1043-1055
- ISSN
- 0892-6638 (ISSN-L)
- 1530-6860
- PMC
- PMC3231946
- OpenAlex
- W2054082659
- Cited by
- 335
- References
- 81
- Citations by year
- 2026: 20 · 2025: 23 · 2024: 14 · 2023: 16 · 2022: 23 · 2021: 32 · 2020: 21 · 2019: 18 · 2018: 7 · 2017: 16 · 2016: 23 · 2015: 25 · 2014: 30 · 2013: 19 · 2012: 24
- FWCI
- 10.25
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- The FASEB Journal (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- U.S. Public Health Service (PO1AG17490)
- Arizona Alzheimer’s Consortium
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Clinical Biochemistry › Advanced Glycation End Products research
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Keywords
- receptor for advanced glycation end products, RAGE signaling, microglia, neuroinflammation, amyloid-beta deposition, Alzheimer's disease, learning and memory impairment, IL-1β, TNF-α, acetylcholinesterase activity, APP transgenic mice, neurotoxicity
- MeSH terms
- Receptor for Advanced Glycation End Products, Alzheimer Disease, Animals, Astrocytes, Disease Models, Animal, Humans, Inflammation, Learning, Memory, Mice, Transgenic, Mutation, Neurons, Tumor Necrosis Factor-alpha, Signal Transduction, Amyloid beta-Peptides, Microglia, Mitogen-Activated Protein Kinases, Mice, Interleukin-1beta
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