The DOI matches its Crossref record; 131 of the 132 references it cites were found in a registry or an index.
Advanced glycation endproducts and their receptor RAGE in Alzheimer's disease
Abstract
Alzheimer's disease (AD) is the most common dementing disorder of late life. Although there might be various different triggering events in the early stages of the disease, they seem to converge on a few characteristic final pathways in the late stages, characterized by inflammation and neurodegeneration. In this review, we revisit the hypothesis that advanced glycation endproducts (AGEs) and their receptor RAGE may play an important role in disease pathogenesis. Accumulation of AGEs in cells and tissues is a normal feature of aging, but is accelerated in AD. In AD, AGEs can be detected in pathological deposits such as amyloid plaques and neurofibrillary tangles. AGEs explain many of the neuropathological and biochemical features of AD such as extensive protein crosslinking, glial induction of oxidative stress and neuronal cell death. Oxidative stress and AGEs initiate a positive feedback loop, where normal age-related changes develop into a pathophysiological cascade. RAGE and its decoy receptor soluble RAGE, may contribute to or protect against AD pathogenesis by influencing transport of β-amyloid into the brain or by manipulating inflammatory mechanisms. Targeted pharmacological interventions using AGE-inhibitors, RAGE-antagonists, RAGE-antibodies, soluble RAGE or RAGE signalling inhibitors such as membrane-permeable antioxidants may be promising therapeutic strategies to slow down the progression of AD.
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“Oxidative stress can also be generated due to AGE formation in the brain. This feed-forward process creates a vicious cycle that exacerbates oxidative damage with the subsequent initiation and progression of neurodegenerative diseases4,103.”
From Advanced glycation end products (AGEs) and other adducts in aging-related diseases and alcohol-mediated tissue injury (2021) · cites this paper as [103]
In the citing paper
“In the brain, AGEs can be produced as a result of elevated oxidative stress during aging or chronic exposure to toxic agents such as alcohol (ethanol), n-6 fatty acid-containing high-fat Western diets, and sugary soft drinks.”
From Advanced glycation end products (AGEs) and other adducts in aging-related diseases and alcohol-mediated tissue injury (2021) · cites this paper as [103]
Citations
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Cited by
Sorted by citations
Mechanisms underlying inflammation in neurodegeneration
Glass, C. K., Saijo, K., Winner, B., Marchetto, M. C., & Gage, F. H. (2010) · Cell · doi:10.1016/j.cell.2010.02.016 · Cited by 3,580
“The increased production of RAGE ligands is often observed in cellular and organ dysfunction, particularly where inflammation is involved (Schmidt et al., 2009; Srikanth et al., 2009).”
Alzheimer Mechanisms and Therapeutic Strategies
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“AGEs generated by hyperglycemia have been identified as a crucial link between diabetes and AD [48-54].”
Metadata
- Authors
- Srikanth, V., Maczurek, A., Phan, T., Steele, M., Westcott, B., Juskiw, D., & Münch, G.
- Affiliations
- Monash University (AU)
- Western Sydney University (AU)
- James Cook University (AU)
- Venue
- Neurobiology of Aging
- Publisher
- Elsevier BV
- Published
- 2011-05
- Volume
- 32
- Issue
- 5
- Pages
- 763-777
- ISSN
- 0197-4580 (ISSN-L)
- OpenAlex
- W2027183895
- Cited by
- 524
- References
- 132
- Citations by year
- 2026: 20 · 2025: 25 · 2024: 31 · 2023: 25 · 2022: 34 · 2021: 46 · 2020: 32 · 2019: 43 · 2018: 26 · 2017: 46 · 2016: 33 · 2015: 39 · 2014: 38 · 2013: 26 · 2012: 32
- FWCI
- 2.34
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- Locations
- Neurobiology of Aging (publishedVersion)
- PubMed (publishedVersion)
- ResearchOnline at James Cook University (James Cook University) (submittedVersion)
- Funders
- National Health and Medical Research Council (436797, 491109)
- Alzheimer's Australia
- Deutsche Forschungsgemeinschaft (Mu 1011/14-1, Mu1011/15-1)
- Alzheimer Forschung Initiative
- Topics
- 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
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Keywords
- advanced glycation end products, RAGE, Alzheimer's disease, soluble RAGE, amyloid plaques, neurofibrillary tangles, oxidative stress, neuroinflammation, neurodegeneration, protein cross-linking, RAGE antagonists, AGE inhibitors, pathogenesis
- MeSH terms
- Receptor for Advanced Glycation End Products, Aging, Alzheimer Disease, Diabetes Mellitus, Type 2, Humans, Macrophages, Receptors, Immunologic, Neurofibrillary Tangles, Glycation End Products, Advanced, Microglia, Oxidative Stress, Disease Progression, Plaque, Amyloid
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