Cited by 335Neuroinflammation and Neurodegeneration MechanismsAdvanced Glycation End Products researchAlzheimer's disease research and treatments

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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

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Fang, Fang, Lue, Lih-Fen, Yan, Shiqiang, Xu, Hongwei, Luddy, John S., Chen, Doris, Walker, Douglas G., Stern, David M., Yan, Shifang, Schmidt, Ann Marie, Chen, John X., Yan, Shirley ShiDu·2010·The FASEB Journal

DOI 10.1096/fj.09-139634PMC PMC3231946

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Abstract

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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See all 335

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
ORCID: Lue, Lih-Fen
Yan, Shiqiang
Xu, Hongwei
Chen, Doris
Walker, Douglas G.
Schmidt, Ann Marie
Venue: The FASEB Journal
Publisher: Wiley
Published: 2009-11-11
Volume: 24
Issue: 4
Pages: 1043-1055
ISSN: 0892-6638 (ISSN-L)
1530-6860
DOI: 10.1096/fj.09-139634
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
Licence: onlinelibrary.wiley.com/termsAndConditions#vor (vor)
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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RAGE‐dependent signaling in microglia contributes to neuroinflammation, Aβ accumulation, and impaired learning/memory in a mouse model of Alzheimer's disease

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