Increased expression of the receptor for advanced glycation end products in neurons and astrocytes in a triple transgenic mouse model of Alzheimer’s disease
Open accessAbstract
The receptor for advanced glycation end products (RAGE) has been reported to have a pivotal role in the pathogenesis of Alzheimer's disease (AD). This study investigated RAGE levels in the hippocampus and cortex of a triple transgenic mouse model of AD (3xTg-AD) using western blotting and immunohistochemical double-labeling to assess cellular localization. Analysis of western blots showed that there were no differences in the hippocampal and cortical RAGE levels in 10-month-old adult 3xTg-AD mice, but significant increases in RAGE expression were found in the 22- to 24-month-old aged 3xTg-AD mice compared with those of age-matched controls. RAGE-positive immunoreactivity was observed primarily in neurons of aged 3xTg-AD mice with very little labeling in non-neuronal cells, with the notable exception of RAGE presence in astrocytes in the hippocampal area CA1. In addition, RAGE signals were co-localized with the intracellular amyloid precursor protein (APP)/amyloid beta (Aβ) but not with the extracellular APP/Aβ. In aged 3xTg-AD mice, expression of human tau was observed in the hippocampal area CA1 and co-localized with RAGE signals. The increased presence of RAGE in the 3xTg-AD animal model showing critical aspects of AD neuropathology indicates that RAGE may contribute to cellular dysfunction in the AD brain.
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RAGE receptors are overexpressed in the BBB and astrocytes, especially in brain tissue from AD animal models and AD patients.
“Our previous research and that of others found that RAGE receptors are overexpressed in the BBB and astrocytes, especially in brain tissue from AD animal models and AD patients.33–35”
From Reverse the progression of Alzheimer’s disease through Nano-ERASER-based adult neuroregeneration (2026) · cites this paper as [35]
The Results (Distribution and cellular localization of RAGE-positive cells; page unavailable) report more RAGE-expressing astrocytes in the hippocampal CA1 region of aged AD-model mice than in controls. The Introduction reports increased RAGE in AD patient brains. The Discussion mentions RAGE-mediated transport across the blood–brain barrier, but does not establish RAGE overexpression at the barrier. (LLM, conf=0.88)
Experimental — accuracy not yet measuredRAGE co-localizes with intracellular APP/Aβ in neurons and human tau in astrocytes in CA1, and its expression increases in the 3xTg-AD mouse model, suggesting RAGE may be involved in AD pathogenesis.
“RAGE co-localizes with intracellular APP/Aβ in neurons, and human tau in astrocytes in the CA1 region, and its expression increases in the 3xTg-AD mouse model, suggesting that RAGE may be involved in AD pathogenesis [409].”
From Molecular and cellular mechanisms underlying the pathogenesis of Alzheimer’s disease (2020) · cites this paper as [409]
RAGEs are expressed widely in various cells and organs.
“Generally, RAGEs are expressed widely in various cells, such as endothelial cells, macrophages/monocytes, neutrophils, lymphocytes, microglia, astrocytes, and neurons, and organs, such as the brain, heart, lung, kidney, and liver36,37.”
From Advanced glycation end products (AGEs) and other adducts in aging-related diseases and alcohol-mediated tissue injury (2021) · cites this paper as [36]
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References 30 · Cited by 111
- Authors
- Choi, B.-R., Cho, W.-H., Kim, J., Lee, H. J., Chung, C., Jeon, W. K., & Han, J.-S.
- Affiliations
- Konkuk University (KR)
- Seoul National University (KR)
- Korea Institute of Oriental Medicine (KR)
- Corresponding author
- Jeon, Won Kyung
- Han, Jung-Soo
- Venue
- Experimental & Molecular Medicine
- Published
- 2014-02-07
- Volume
- 46
- Issue
- 2
- Pages
- e75-e75
- ISSN
- 1226-3613 (ISSN-L)
- 2092-6413
- PMC
- PMC3909893
- OpenAlex
- W2065326233
- Cited by
- 111
- References
- 30
- Citations by year
- 2026: 6 · 2025: 7 · 2024: 5 · 2023: 4 · 2022: 18 · 2021: 9 · 2020: 13 · 2019: 12 · 2018: 7 · 2017: 11 · 2016: 5 · 2015: 12 · 2014: 2
- FWCI
- 6.89
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- cc-by-nc-sa
- www.springer.com/tdm (unspecified)
- Locations
- Experimental & Molecular Medicine (publishedVersion, cc-by-nc-sa)
- Europe PMC (PubMed Central) (publishedVersion, cc-by-nc-sa)
- PubMed Central (publishedVersion, cc-by-nc-sa)
- PubMed (publishedVersion)
- Funders
- Korea Research Council of Fundamental Science and Technology
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Clinical Biochemistry › Advanced Glycation End Products research
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Keywords
- receptor for advanced glycation end products, RAGE, Alzheimer's disease, triple transgenic mouse model, 3xTg-AD mice, neurons, astrocytes, hippocampus, amyloid-beta, amyloid precursor protein, tau protein, CA1, aging, neurodegeneration
- MeSH terms
- Receptor for Advanced Glycation End Products, Alzheimer Disease, Animals, Astrocytes, Humans, Mice, Transgenic, Neurons, Receptors, Immunologic, Amyloid beta-Peptides, tau Proteins, Mice, CA1 Region, Hippocampal
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