The DOI matches its Crossref record; 81 of the 81 references it cites were found in a registry or an index.
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
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
In the citing paper
“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]
In the citing paper
“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]
In the citing paper
“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]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Inflammation and Alzheimer’s disease
Akiyama, H. (2000) · Neurobiology of Aging · doi:10.1016/s0197-4580(00)00124-x · Cited by 4,514
RAGE and amyloid-β peptide neurotoxicity in Alzheimer's disease
Yan, S. D., Chen, X., Fu, J., Chen, M., Zhu, H., Roher, A., Slattery, T., Zhao, L., Nagashima, M., Morser, J., et al. (1996) · Nature · doi:10.1038/382685a0 · Cited by 2,012
Self-citationRAGE Mediates a Novel Proinflammatory Axis
Hofmann, M. A., Drury, S., Fu, C., Qu, W., Taguchi, A., Lu, Y., Avila, C., Kambham, N., Bierhaus, A., Nawroth, P., et al. (1999) · Cell · doi:10.1016/s0092-8674(00)80801-6 · Cited by 1,864
Self-citationFarris, W., Mansourian, S., Chang, Y., Lindsley, L., Eckman, E. A., Frosch, M. P., Eckman, C. B., Tanzi, R. E., Selkoe, D. J., & Guénette, S. Y. (2003) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0230450100 · Cited by 1,526
RAGE mediates amyloid-β peptide transport across the blood-brain barrier and accumulation in brain
Deane, R., Du Yan, S., Submamaryan, R. K., LaRue, B., Jovanovic, S., Hogg, E., Welch, D., Manness, L., Lin, C., Yu, J., et al. (2003) · Nature Medicine · doi:10.1038/nm890 · Cited by 1,426
Self-citationABAD Directly Links Aß to Mitochondrial Toxicity in Alzheimer's Disease
Lustbader, J. W., Cirilli, M., Lin, C., Xu, H. W., Takuma, K., Wang, N., Caspersen, C., Chen, X., Pollak, S., Chaney, M., et al. (2004) · Science · doi:10.1126/science.1091230 · Cited by 1,303
Self-citationWyss-Coray (2006) · doi:10.1038/nm1484 · Cited by 1,284
Mechanisms of Neuronal Degeneration in Alzheimer's Disease
Yankner, B. A. (1996) · Neuron · doi:10.1016/s0896-6273(00)80115-4 · Cited by 953
Du, H., Guo, L., Fang, F., Chen, D., Sosunov, A. A., McKhann, G. M., Yan, Y., Wang, C., Zhang, H., Molkentin, J. D., et al. (2008) · Nature Medicine · doi:10.1038/nm.1868 · Cited by 950
Self-citationEl Khoury, J., Toft, M., Hickman, S. E., Means, T. K., Terada, K., Geula, C., & Luster, A. D. (2007) · Nature Medicine · doi:10.1038/nm1555 · Cited by 915
Flagged first, then by citations
Cited by
Sorted by citations
Sterile inflammation: sensing and reacting to damage
Chen, G. Y., & Nuñez, G. (2010) · Nature Reviews Immunology · doi:10.1038/nri2873 · Cited by 3,051
Microglia development and function
Nayak, D., Roth, T. L., & McGavern, D. B. (2014) · Annual Review of Immunology · doi:10.1146/annurev-immunol-032713-120240 · Cited by 1,154
Molecular and cellular mechanisms underlying the pathogenesis of Alzheimer’s disease
Guo, T., Zhang, D., Zeng, Y., Huang, T. Y., Xu, H., & Zhao, Y. (2020) · Molecular Neurodegeneration · doi:10.1186/s13024-020-00391-7 · Cited by 994
Self-citationFranceschi, C., Garagnani, P., Vitale, G., Capri, M., & Salvioli, S. (2017) · Trends in Endocrinology & Metabolism · doi:10.1016/j.tem.2016.09.005 · Cited by 997
The biphasic function of microglia in ischemic stroke
Ma, Y., Wang, J., Wang, Y., & Yang, G.-Y. (2017) · Progress in Neurobiology · doi:10.1016/j.pneurobio.2016.01.005 · Cited by 655
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
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
