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 be generated due to AGE formation in the brain; this feed-forward process creates a vicious cycle that exacerbates oxidative damage with subsequent initiation and progression of neurodegenerative diseases.
“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 brain, AGEs can be produced as a result of elevated oxidative stress during aging or chronic exposure to toxic agents such as alcohol, n-6 fatty acid-containing high-fat Western diets, and sugary soft drinks.
“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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Self-citationAre advanced glycation end-products associated with amyloidosis in Alzheimer’s disease?
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Self-citationAmyloidosis, advanced glycation end products and Alzheimer disease
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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 · see citing works
“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
Huang, Y., & Mucke, L. (2012) · Cell · doi:10.1016/j.cell.2012.02.040 · Cited by 1,758 · see citing works
HMGB1 and RAGE in Inflammation and Cancer
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“AGEs generated by hyperglycemia have been identified as a crucial link between diabetes and AD [48-54].”
Is Alzheimer’s disease a type 3 diabetes? A critical appraisal
Kandimalla, R., Thirumala, V., & Reddy, P. H. (2017) · Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease · doi:10.1016/j.bbadis.2016.08.018 · Cited by 621 · see citing works
“AGE also causes the stimulation of TNF-α which in turn acceleratesβ-secretase (BACE) expression further causing APP processing for the formation of Aβ in astrocytes of diabetic models of AD [93,94].”
Brain Atrophy in Type 2 Diabetes
Moran, C., Phan, T. G., Chen, J., Blizzard, L., Beare, R. J., Venn, A., Münch, G. W., WOOD, A. G., Forbes, J. M., Greenaway, T. M., et al. (2013) · Diabetes Care · doi:10.2337/dc13-0143 · Cited by 521 · see citing works
“Chronic hyperglycemia increases the formation of advanced glycation end products, which promote oxidative stress, cross-linking of amyloid fibrils, modification of cytoskeletal tau proteins, and inflammation (36).”
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Microglia during development and aging
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“Increased production of these ligands is observed with cellular dysfunction and inflammation (Schmidt et al., 2009; Srikanth et al., 2011).”
BackgroundType 2 diabetes and cognitive dysfunction–towards effective management of both comorbidities
Srikanth, V., Sinclair, A. J., Hill-Briggs, F., Moran, C., & Biessels, G. J. (2020) · The Lancet Diabetes & Endocrinology · doi:10.1016/s2213-8587(20)30118-2 · Cited by 465 · see citing works
Self-citationA synopsis on aging—Theories, mechanisms and future prospects
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The Ketogenic Diet as a Treatment Paradigm for Diverse Neurological Disorders
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The contribution of neuroinflammation to amyloid toxicity in Alzheimer's disease
Minter, M. R., Taylor, J. M., & Crack, P. J. (2016) · Journal of Neurochemistry · doi:10.1111/jnc.13411 · Cited by 451 · see citing works
“Receptor for advanced glycated end-products are expressed on microglia and detect amino groups of peptides that have undergone glycation and oxidation reactions, making them critical Ab sensors that lead to production of a milieu of pro-inflammatory cytokines (Srikanth et al. 2011).”
BackgroundRungratanawanich, W., Qu, Y., Wang, X., Essa, M. M., & Song, B.-J. (2021) · Experimental & Molecular Medicine · doi:10.1038/s12276-021-00561-7 · Cited by 411 · see citing works
Defective mitophagy in Alzheimer’s disease
Pradeepkiran, J. A., & Reddy, P. H. (2020) · Ageing Research Reviews · doi:10.1016/j.arr.2020.101191 · Cited by 367 · see citing works
“Oxidative stress and neuronal inflammation caused by AGE-RAGE and/or RAGE-Aβ interactions lead to defective autophagy and mitophagy (Srikanth et al., 2011).”
BackgroundByun, K., Yoo, Y., Son, M., Lee, J., Jeong, G.-B., Park, Y. M., Salekdeh, G. H., & Lee, B. (2017) · Pharmacology & Therapeutics · doi:10.1016/j.pharmthera.2017.02.030 · Cited by 357 · see citing works
“AGEs can induce the development or progression of not only diabetic complications but the pathophysiologies of many diseases, including cardiovascular diseases (CVDs) and neurodegenerative diseases like Alzheimer's disease (AD), Parkinson's disease (PD), and alcoholic brain damage (Bayarsaikhan et al., 2016; Byun et a…”
Sharma, P., Srivastava, P., Seth, A., Tripathi, P. N., Banerjee, A. G., & Shrivastava, S. K. (2019) · Progress in Neurobiology · doi:10.1016/j.pneurobio.2018.12.006 · Cited by 331 · see citing works
Features of Microglia and Neuroinflammation Relevant to Environmental Exposure and Neurotoxicity
Kraft, A. D., & Harry, G. J. (2011) · International Journal of Environmental Research and Public Health · doi:10.3390/ijerph8072980 · Cited by 330 · see citing works
“Increased production of these ligands is observed with cellular dysfunction and inflammation [72,73].”
BackgroundKetogenic Diet in Alzheimer’s Disease
Rusek, M., Pluta, R., Ułamek-Kozioł, M., & Czuczwar, S. J. (2019) · International Journal of Molecular Sciences · doi:10.3390/ijms20163892 · Cited by 319 · see citing works
“The altered glucose metabolism and mitochondrial function may result from the accumulation of advanced glycation end products (AGEs) [85].”
BackgroundAdvanced glycation end products and neurodegenerative diseases: Mechanisms and perspective
Li, J., Liu, D., Sun, L., Lu, Y., & Zhang, Z. (2012) · Journal of the Neurological Sciences · doi:10.1016/j.jns.2012.02.018 · Cited by 320 · see citing works
“Therefore, AGEs are recognized to play an important role in the development of AD and other neurodegenerative diseases [6].”
BackgroundMicroglia in Alzheimer’s disease: pathogenesis, mechanisms, and therapeutic potentials
Miao, J., Ma, H., Yang, Y., Liao, Y., Lin, C., Zheng, J., Yu, M., & Lan, J. (2023) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2023.1201982 · Cited by 293 · see citing works
“Oligomeric Aβ strongly activates RAGE in neurons and microglia, which leads to neurodegeneration (Yan et al., 2009; Origlia et al., 2010; Srikanth et al., 2011).”
BackgroundRehman, S. U., Shah, S. A., Ali, T., Chung, J. I., & Kim, M. O. (2016) · Molecular Neurobiology · doi:10.1007/s12035-015-9604-5 · Cited by 285 · see citing works
Oxidative stress and β-amyloid protein in Alzheimer’s disease
Cai, Z., Zhao, B., & Ratka, A. (2011) · NeuroMolecular Medicine · doi:10.1007/s12017-011-8155-9 · Cited by 279 · see citing works
“In BBB, oxidative stress decreases the expression of low-density lipoprotein receptor-related protein 1 (LRP-1) and up-regulates the receptor for advanced glycation end products (RAGE) and increases its permeability, which could potentially lead to increased deposition of Ab within the AD brain (Deane et al. 2004; Jey…”
BackgroundInfluentialInsulin Resistance and Alzheimer’s Disease: Bioenergetic Linkages
Neth, B. J., & Craft, S. (2017) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2017.00345 · Cited by 275 · see citing works
“AGEs are also more elevated in adults with AD than age-matched controls and may ultimately contribute to AD pathology (Sasaki et al., 1998; Srikanth et al., 2011).”
BackgroundAlzheimer's disease and type 2 diabetes: a critical assessment of the shared pathological traits
Chatterjee, S., & Mudher, A. (2018) · Frontiers in Neuroscience · doi:10.3389/fnins.2018.00383 · Cited by 270 · see citing works
Ali, T., Badshah, H., Kim, T. H., & Kim, M. O. (2014) · Journal of Pineal Research · doi:10.1111/jpi.12194 · Cited by 269 · see citing works
“Overexpressed RAGE activates NF-KB, results in the activation of other inflammatory mediators and glial activation, which results in progressive age-related diseases such as type II diabetes, atherosclerosis, and other chronic neurodegenerative diseases including AD and Parkinson disease [49, 50].”
BackgroundThe biological pathways of Alzheimer disease: a review
Calabrò, M., Rinaldi, C., Santoro, G., & Crisafulli, C. (2020) · AIMS neuroscience · doi:10.3934/neuroscience.2021005 · Cited by 271 · see citing works
“Their expression also tends to increase naturally with age, offering a possible explanation for the increased risk to AD with Age [243,244,247].”
BackgroundPaudel, Y. N., Angelopoulou, E., Piperi, C., Othman, I., Aamir, K., & Shaikh, M. F. (2020) · Cells · doi:10.3390/cells9020383 · Cited by 257 · see citing works
Insulin Resistance and Oxidative Stress in the Brain: What’s New?
Maciejczyk, M., Żebrowska, E., & Chabowski, A. (2019) · International Journal of Molecular Sciences · doi:10.3390/ijms20040874 · Cited by 262 · see citing works
“overproduction as well as neuronal inflammation [102,116,119].”
BackgroundOxidative Stress Signaling to Chromatin in Health and Disease
Kreuz, S., & Fischle, W. (2016) · Epigenomics · doi:10.2217/epi-2016-0002 · Cited by 254 · see citing works
Pathophysiology of RAGE in inflammatory diseases
Dong, H., Zhang, Y., Huang, Y., & Deng, H. (2022) · Frontiers in Immunology · doi:10.3389/fimmu.2022.931473 · Cited by 245 · see citing works
Receptor for Advanced Glycation End Products and Its Involvement in Inflammatory Diseases
Chuah, Y. K., Basir, R., Talib, H., Tie, T. H., & Nordin, N. (2013) · International Journal of Inflammation · doi:10.1155/2013/403460 · Cited by 243 · see citing works
RAGE in tissue homeostasis, repair and regeneration
Sorci, G., Riuzzi, F., Giambanco, I., & Donato, R. (2012) · Biochimica et Biophysica Acta (BBA) - Molecular Cell Research · doi:10.1016/j.bbamcr.2012.10.021 · Cited by 229 · see citing works
“Indeed, the participation of RAGE signaling in neurodegenerative diseases via direct effects on neurons and indirect effects through microglia and astrocyte activation is long recognized [17,80,81].”
BackgroundKetogenic Diet in Neuromuscular and Neurodegenerative Diseases
Paoli, A., Bianco, A., Damiani, E., & Bosco, G. (2014) · BioMed Research International · doi:10.1155/2014/474296 · Cited by 221 · see citing works
“There is another pathophysiological mechanism ascribed to an altered mitochondrial function and glucose metabolism in AD: the accumulation of advanced glycation end products (AGEs) [83].”
BackgroundAssociation of type 2 diabetes with brain atrophy and cognitive impairment
Roberts, R. O., Knopman, D. S., Przybelski, S. A., Mielke, M. M., Kantarci, K., Preboske, G. M., Senjem, M. L., Pankratz, V. S., Geda, Y. E., Boeve, B. F., et al. (2014) · Neurology · doi:10.1212/wnl.0000000000000269 · Cited by 211 · see citing works
Berberine and neurodegeneration: A review of literature
Ahmed, T., Gilani, A. H., Abdollahi, M. R., Daglia, M., Nabavi, S. F., & Nabavi, S. M. (2015) · Pharmacological Reports · doi:10.1016/j.pharep.2015.03.002 · Cited by 210 · see citing works
“lipopolysaccharide stimulated murine macrophages by inhibiting iNOS expression [37].”
BackgroundDing, B., Lin, C., Liu, Q., He, Y., Ruganzu, J. B., Jin, H., Peng, X., Ji, S., Ma, Y., & Yang, W. (2020) · Journal of Neuroinflammation · doi:10.1186/s12974-020-01981-4 · Cited by 208 · see citing works
“Binding of Aβ to RAGE activates a signaling cascade that leads to the activation of the transcription factor NFκB, which augments the transcription of various proinflammatory cytokines (TNF-α, IL-6, and IL-1β) and enhances microglia and astrocyte activation [7, 42].”
BackgroundAGEs induce Alzheimer-like tau pathology and memory deficit via RAGE-mediated GSK-3 activation
Li, X., Lv, B.-L., Xie, J., Liu, J., Zhou, X., & Wang, J. (2011) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2011.02.003 · Cited by 207 · see citing works
“The intracellular AGEs may influence the structural inegrity of the cells through direct cross-linking, while the xtracellular AGEs may induce biological effects through inding to specific cell surface molecules, such as RAGE Srikanth et al., 2009).”
InfluentialBrkic, M., Balusu, S., Libert, C., & Vandenbroucke, R. E. (2015) · Mediators of Inflammation · doi:10.1155/2015/620581 · Cited by 205 · see citing works
“Activation of the receptor for AGE (RAGE) leads to release of proinflammatory cytokines and free radicals, further contributing to inflammatory processes [135].”
BackgroundMolecular Mechanisms and Genetics of Oxidative Stress in Alzheimer’s Disease
Cioffi, F., Adam, R. H. I., & Broersen, K. (2019) · Journal of Alzheimer s Disease · doi:10.3233/jad-190863 · Cited by 204 · see citing works
“The roles of RAGE and AGEs in AD pathogenesis have been covered in a number of reviews [426, 427].”
BackgroundRedox Signaling and Advanced Glycation Endproducts (AGEs) in Diet-Related Diseases
Cepas, V., Collino, M., Mayo, J. C., & Sainz, R. M. (2020) · Antioxidants · doi:10.3390/antiox9020142 · Cited by 206 · see citing works
“For this reason, AGEs are recognized as important players in the pathogenesis of several neurodegenerative disorders such as Alzheimer’s or Parkinson’s diseases [145,146], but also Huntington’s disease, amyotrophic lateral sclerosis or Creutzfeldt-Jakob disease [147,148].”
BackgroundMolecular links between Alzheimer’s disease and diabetes mellitus
Yang, Y., & Song, W. (2013) · Neuroscience · doi:10.1016/j.neuroscience.2013.07.009 · Cited by 201 · see citing works
Ketone Bodies in Neurological Diseases: Focus on Neuroprotection and Underlying Mechanisms
Yang, H.-J., Wei, S., Zhu, F., Wu, J.-P., & Wang, Q. (2019) · Frontiers in Neurology · doi:10.3389/fneur.2019.00585 · Cited by 187 · see citing works
“The accumulation of AGE during healthy aging accelerates the progression of AD.”
BackgroundMitochondrial dysfunction in Alzheimer’s disease
D’Alessandro, M. C. B., Kanaan, S., Geller, M., Praticò, D., & Daher, J. P. L. (2025) · Ageing Research Reviews · doi:10.1016/j.arr.2025.102713 · Cited by 201 · see citing works
“The accumulation of advanced glycation end products (AGEs) and their interaction with the receptor for AGEs (RAGE) represent another critical pathway linking metabolic dysregulation impaired insulin signaling and mitochondrial dysfunction in AD (Srikanth et al., 2011).”
Ullah, F., Ali, T., Ullah, N., & Kim, M. O. (2015) · Neurochemistry International · doi:10.1016/j.neuint.2015.07.001 · Cited by 199 · see citing works
“AGE level increases with aging and pathologically has been implicated in various age-associated disorders such as atheriosclerosis, nephropathy, diabetes and AD (Bayens, 2001; Srikanth et al., 2009).”
Münch, G. W., Venigalla, M., Sonego, S., & Gyengési, E. (2015) · Neural Regeneration Research · doi:10.4103/1673-5374.162686 · Cited by 193 · see citing works
“…to be mediated by its transport across the blood-brain barrier by the receptor for advanced glycation end products and efflux via the multi-ligand lipoprotein receptor LRP-1 and it is suggested that this process is impaired in sporadic AD patients (Bates et al., 2009; Srikanth et al., 2011).”
Self-citationAlzheimer's Disease: Redox Dysregulation As a Common Denominator for Diverse Pathogenic Mechanisms
Rommy von Bernhardi, M., & Eugenín, J. L. (2011) · Antioxidants and Redox Signaling · doi:10.1089/ars.2011.4082 · Cited by 189 · see citing works
“In astrocytes, AGE-conjugated proteins form granules, suggesting that astrocytes uptake and degrade glycated proteins (598).”
BackgroundMeasuring gait speed to better identify prodromal dementia
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“Cromoglicic acid Approved (alternate indication) ALZT-OP1 Approved (alternate indication) CHF 5074 Phase 2 RAGE Antagonists (Srikanth et al., 2011; Gilham et al., 2016) RAGE increases pathogenic pro-inflammatory signaling in diabetes, AD, and cancer.”
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“Advanced glycation end products are markers of carbonyl stress and formed in excess during ageing and diabetes mellitus (Wautier and Guillausseau, 2002; Srikanth et al., 2009).”
BackgroundA New Link to Mitochondrial Impairment in Tauopathies
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“The authors hypothesize that a significant expression of RAGE and one of its ligands HMGB1 in microglia could amplify the inflammatory response in MS (Andersson et al. 2008).”
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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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“There are various RAGE ligands including AGEs, S100 proteins, and amphoterins [91, 92].”
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“A RAGE inhibitor (PF-04494700) has completed phase 2.”
InfluentialRAGE-TLR Crosstalk Sustains Chronic Inflammation in Neurodegeneration
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“This unveils deleterious effects of robust RAGE activation and amplifies and perpetuates the inflammatory reactions [11, 89, 90, 96].”
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“Glycation of tau protein promotes production of NFT (Srikanth et al. 2011).”
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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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“AGEs have been implicated as causal factors for a wide range of diseases, in particular for type 2 diabetes [217,218] and also for memory decline and Alzheimer’s disease [219,220].”
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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).”
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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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“Binding of AGEs or Ab to RAGE activates the NF-jB pathway, which is involved in the regulation of the expression of inflammatory cytokines, such as tumor necrosis factor-a (TNF-a) and interleukin-1beta (IL-1b) [6, 32], NF-jB activation also upregulates RAGE expression [33].”
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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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Lifestyle and clinical determinants of skin autofluorescence in a population‐based cohort study
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- 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
- Health Sciences › Medicine › Physiology › 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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