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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]
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“Several studies characterized AGEs and the related receptor (RAGE) in AD [17], but data in PD patients are scarce.”
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Novel insights for the treatment of Alzheimer's disease
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“A RAGE inhibitor (PF-04494700) has completed phase 2.”
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“Glycation of tau protein promotes production of NFT (Srikanth et al. 2011).”
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Prediabetes Is Associated With Structural Brain Abnormalities: The Maastricht Study
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“Srikanth et al. (2011) claimed that AGE accumulation in cells and tissues is a normal feature of aging that is accelerated in AD and that AGE and RAGE can play an important role in the pathogenesis of AD because they are found in pathological deposits such as amyloid plaques and neurofibrillary…”
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“Evidence shows that AGEs is a harmless post-translational protein modification and it can accelerate the aging process (Srikanth et al., 2009).”
InfluentialTransient dynamics of Aβ contribute to toxicity in Alzheimer’s disease
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Methylglyoxal, Cognitive Function and Cerebral Atrophy in Older People
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“Research has also demonstrated that exposure to ultraviolet radiation A (UVA) in the presence of AGEs triggers the generation of ROS such as superoxide, hydrogen peroxide, and hydroxyl radicals.”
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InfluentialRegional Brain Gray Matter Changes in Patients with Type 2 Diabetes Mellitus
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“Second, HNPs exposed to S100B or Ab42 dosed-dependently increased GFAP and decreased MAP2 expression; concurrent exposure of S100B and Ab42 enhanced GFAP and inhibited MAP2 expression synergistically (Figure 4B).”
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Kidney, heart and brain: three organs targeted by ageing and glycation
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Lifestyle and clinical determinants of skin autofluorescence in a population‐based cohort study
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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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