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.
Overview
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
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
“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
Cites
High-mobility group box 1 protein (HMGB1): nuclear weapon in the immune arsenal
Lotze, M. T., & Tracey, K. J. (2005) · Nature reviews. Immunology · doi:10.1038/nri1594 · Cited by 2,490
Diabetes mellitus and the risk of dementia: The Rotterdam Study
Ott, A., Stolk, R. P., van Harskamp, F., Pols, H. A. P., Hofman, A., & Breteler, M. M. B. (1999) · Neurology · doi:10.1212/wnl.53.9.1937 · Cited by 2,175
Copper, iron and zinc in Alzheimer's disease senile plaques
Lovell, M. A., Robertson, J. D., Teesdale, W. J., Campbell, J. L., & Markesbery, W. R. (1998) · Journal of the Neurological Sciences · doi:10.1016/s0022-510x(98)00092-6 · Cited by 2,120
Hydrogen peroxide mediates amyloid β protein toxicity
Behl, C. (1994) · Cell · doi:10.1016/0092-8674(94)90131-7 · Cited by 2,074
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
Donato, R. (2001) · The International Journal of Biochemistry & Cell Biology · doi:10.1016/s1357-2725(01)00046-2 · Cited by 1,580
Neeper, M. P., Schmidt, A. M., Brett, J., Yan, S. D., Wang, F., Pan, Y., Elliston, K. O., Stern, D., & SHAW, A. R. (1992) · Journal of Biological Chemistry · doi:10.1016/s0021-9258(18)42138-2 · Cited by 1,545
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
Microglial Dysfunction and Defective β-Amyloid Clearance Pathways in Aging Alzheimer's Disease Mice
Hickman, S. E., Allison, E. K., & El Khoury, J. (2008) · The Journal of Neuroscience · doi:10.1523/jneurosci.0616-08.2008 · Cited by 1,329
Advanced protein glycosylation in diabetes and aging
Brownlee, M. D. (1995) · Annual Review of Medicine · doi:10.1146/annurev.med.46.1.223 · Cited by 1,312
Research works printed but not linked: 2
- Dukic-Stefanovic, 2003, Signal transduction pathways in mouse microglia N-11 cells activated by advanced glycation endproducts (AGEs), J. Neurochem., 87, 44, 10.1046/j.1471-4159.2003.01988.x · DOI
- Yan, 1996, RAGE and amyloid-beta peptide neurotoxicity in Alzheimer's disease, Nature, 382, 685, 10.1038/382685a0 · DOI · Paper page
Cited by
Sorted by citations
Items 301–400 of 526
Liu, H., Chen, J., Ling, J., Wu, Y., Yang, P., Liu, X., Liu, J., Zhang, D., Yin, X., Yu, P., et al. (2024) · International Journal of Surgery · doi:10.1097/js9.0000000000002156 · Cited by 19
Contribution of hyperglycemia-induced changes in microglia to Alzheimer’s disease pathology
Rodríguez, M. H., Flores‐Clemente, C., Macías-Pérez, M. E., Rodríguez-Fonseca, R. A., Nicolás‐Vázquez, M. I., Martínez, J. O., Miranda, R., Rosas, M., & Jiménez, E. M. (2022) · Pharmacological Reports · doi:10.1007/s43440-022-00405-9 · Cited by 17
“AGEs induce the expression of RAGE in several brain cells [135].”
BackgroundChiang, M., Cheng, Y., Nicol, C. J. B., & Lin, C. (2017) · The International Journal of Biochemistry & Cell Biology · doi:10.1016/j.biocel.2017.09.020 · Cited by 17
Investigation Into the Effects of Tenilsetam on Markers of Neuroinflammation in GFAP-IL6 Mice
Gyengési, E., Liang, H., Millington, C., Sonego, S., Sirijovski, D., Gunawardena, D., Dhananjayan, K., Venigalla, M., Niedermayer, G., & Münch, G. W. (2018) · Pharmaceutical Research · doi:10.1007/s11095-017-2326-9 · Cited by 16
“A decrease in AGE formation might lower total AGE levels, and thereby decreasing proinflammatory activation of the AGE receptor RAGE (31,32).”
BackgroundSelf-citationLi, Z., Yang, P., & Feng, B. (2020) · Molecular Biology Reports · doi:10.1007/s11033-020-05998-z · Cited by 16
Potential new therapeutic target for Alzheimer's disease: Glucagon‐like peptide‐1
Liu, X., Zhang, N., Zhang, S., & Xu, P. (2021) · European Journal of Neuroscience · doi:10.1111/ejn.15502 · Cited by 16
Ali, M. Y., Jung, H. A., Jannat, S., & Choi, J. S. (2017) · Archives of Pharmacal Research · doi:10.1007/s12272-017-0999-6 · Cited by 16
Antioxidants as Potential Therapeutics in Neurodegeneration
Sharma, S. K., & Ebadi, M. (2014) · Springer eBooks · doi:10.1007/978-3-642-30018-9_85 · Cited by 15
Rock, C. A., Keeney, S. J., Zakharchenko, A., Takano, H., Spiegel, D. A., Krieger, A. Μ., Ferrari, G. M., & Levy, R. J. (2021) · Acta Biomaterialia · doi:10.1016/j.actbio.2020.12.053 · Cited by 15
Chakraborty, A., Sami, S. A., & Marma, K. K. S. (2021) · The Egyptian Journal of Internal Medicine · doi:10.1186/s43162-021-00081-w · Cited by 18
“RAGE and its role in oxidative stress Oxidative stress is induced due to an imbalance of free radical production and detoxification [8].”
BackgroundGrasset, L., Frison, É., Helmer, C., Catheline, G., Chêne, G., & Dufouil, C. (2024) · European Journal of Epidemiology · doi:10.1007/s10654-023-01080-7 · Cited by 15
Gasparotto, J., Senger, M. R., Kunzler, A., Degrossoli, A., De-Simone, S. G., Bortolin, R. C., Somensi, N., Girardi, C. S., de Souza, C. D. S. F., Calabrese, K. D. S., et al. (2014) · Brain Behavior and Immunity · doi:10.1016/j.bbi.2014.06.204 · Cited by 16
“The receptor for advanced glycation endproducts (RAGE) is a multiligand membrane receptor that exerts crucial roles in the development of chronic inflammatory processes (Srikanth et al., 2011).”
Igase, M., Ohara, M., Igase, K., Kato, T., Okada, Y., Ochi, M., Tabara, Y., Kohara, K., & Ohyagi, Y. (2016) · Journal of Alzheimer s Disease · doi:10.3233/jad-160917 · Cited by 16
“Accumulation of AGEs in cells and tissues is a normal feature of aging but is accelerated in AD [4], suggesting a contribution of AGEs to the pathogenesis of dementia.”
Chambers, A., Bury, J. J., Minett, T., Richardson, C. D., Brayne, C., Ince, P. G., Shaw, P. J., Garwood, C. J., Heath, P. R., Simpson, J. E., et al. (2020) · Journal of Neuropathology & Experimental Neurology · doi:10.1093/jnen/nlaa064 · Cited by 15
Eva, T. A., Barua, N., Chowdhury, M. M., Yeasmin, S., Rakib, A., Islam, M. R., Emran, T. B., & Simal‐Gándara, J. (2020) · Critical Reviews in Food Science and Nutrition · doi:10.1080/10408398.2020.1856771 · Cited by 15
Understanding the Aging Process Using Epidemiologic Approaches
Sanders, J. L., Boudreau, R. M., Newman, A. B., Newman, A. B., & Newman, A. B. (2012) · Springer eBooks · doi:10.1007/978-94-007-5061-6_12 · Cited by 15
Advanced Glycation Endproducts Interfere with Adhesion and Neurite Outgrowth
Bennmann, D., Horstkorte, R., Hofmann, B., Jacobs, K. E., Santos, A. N., Simm, A., Bork, K., & Gnanapragassam, V. S. (2014) · PLoS ONE · doi:10.1371/journal.pone.0112115 · Cited by 15
“This is of special interest since AGE-modified proteins had been already detected in ß-amyloid plaques of Alzheimer patients [29].”
BackgroundNi, Z., Zhuge, Z., Li, W., Xu, H., Zhang, Z., & Dai, H. (2012) · Biological and Pharmaceutical Bulletin · doi:10.1248/bpb.b12-00249 · Cited by 15
Reprint of “Accumulation of modified proteins and aggregate formation in aging”
Nowotny, K., Jung, T., Grune, T., & Höhn, A. (2014) · Experimental Gerontology · doi:10.1016/j.exger.2014.10.001 · Cited by 15
“For example, AGEs are involved in the genesis of neurodegenerative diseases including AD and PD (Li J. et al., 2012; Srikanth et al., 2011).”
BackgroundRen, L., & Yan, H. (2021) · Clinics and Research in Hepatology and Gastroenterology · doi:10.1016/j.clinre.2021.101792 · Cited by 14
Watanabe, M., Toyomura, T., Wake, H., Nishinaka, T., Hatipoğlu, Ö. F., Takahashi, H. K., Nishibori, M., & Mori, S. (2022) · Molecular Biology Reports · doi:10.1007/s11033-021-07096-0 · Cited by 14
d-ribose-mediated glycation of fibrinogen: Role in the induction of adaptive immune response
Alouffi, S., Khanam, A., Husain, A., Akasha, R., Rabbani, G., & Ahmad, S. (2022) · Chemico-Biological Interactions · doi:10.1016/j.cbi.2022.110147 · Cited by 16
Unveiling new secrets in Parkinson’s disease: The glycatome
Chegão, A., & Miranda, H. V. (2023) · Behavioural Brain Research · doi:10.1016/j.bbr.2023.114309 · Cited by 15
“RAGE has been linked to several pathological conditions, such as diabetes complications, chronic inflammation, cancer, and neurodegenerative diseases such as PD [57, 63-66].”
Putranto, E. W., Murata, H., Yamamoto, K., Kataoka, K., Yamada, H., Futami, J., Sakaguchi, M., & Huh, N. (2013) · International Journal of Molecular Medicine · doi:10.3892/ijmm.2013.1467 · Cited by 14
“…the increased expression of RAGE potentially lead to inflam-mation-associated pathological conditions, such as those found in neurodegenerative diseases (8,15,16), cardiovascular and renal diseases (17,18), pulmonary diseases (19), diabetes and metabolic disorders (20,21), as well as cancer (22).”
Natural Compounds (Small Molecules) as Potential and Real Drugs of Alzheimer's Disease
Cahlíková, L., Macáková, K., Benešová, N., Chlebek, J., Hošťálková, A., & Opletal, L. (2014) · Studies in natural products chemistry · doi:10.1016/b978-0-444-63281-4.00006-9 · Cited by 14
From Fork to Brain: The Role of AGE–RAGE Signaling and the Western Diet in Neurodegenerative Disease
Pomroy, H. J., Mote, A., Mathew, S., Chanasseril, S., Lu, V., & Cheema, A. K. (2025) · NeuroSci · doi:10.3390/neurosci6030089 · Cited by 13
“…AGEs did not cross the gastrointestinal barrier and enter our bloodstream, meaning AGEs had no or little impact [21], compelling evidence now shows that reducing dietary AGEs can improve blood sugar regulation and reduce inflammation, particularly in patients with diabetes or renal disease [22,23].”
Akhter, F., Akhter, A., Zhu, X., Schiff, H. C., Maffei, A., Douglas, J. T., Zhou, Q., Zhao, Z., & Zhu, D. (2025) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.2505046122 · Cited by 16
“…of gA β to substrates or its binding to surface receptors, such as receptor for AGE (RAGE), leads to neuroinflammation and synaptic toxicity ( 7 ). gA β with the altered secondary structure is a more suitable ligand than authentic A β for RAGE, resulting in the subsequent activation of…”
Ham, H. J., Lee, Y. S., Koo, J. K., Yun, J., Son, D. J., Han, S., & Hong, J. T. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms25105550 · Cited by 13
Watanabe, M., Toyomura, T., Tomiyama, M., Wake, H., Liu, K., Teshigawara, K., Takahashi, H. K., Nishibori, M., & Mori, S. (2020) · Molecular Biology Reports · doi:10.1007/s11033-020-05783-y · Cited by 13
Ghavipanje, N., Nasri, M. H. F., & Vargas‐Bello‐Pérez, E. (2022) · Journal of Animal Physiology and Animal Nutrition · doi:10.1111/jpn.13769 · Cited by 13
Zabetian‐Targhi, F., Srikanth, V. K., Smith, K. J., Oddy, W. H., Beare, R. J., Moran, C., Wang, W., & Callisaya, M. L. (2019) · Journal of Nutrition · doi:10.1093/jn/nxz139 · Cited by 13
Self-citationAbidar, S., Yıldız, O., Değirmenci, A., Amakran, A., Maadoudi, M. E., & Nhiri, M. (2019) · Journal of Food Biochemistry · doi:10.1111/jfbc.13009 · Cited by 13
Edler, M. K., Johnson, C. T., Ahmed, H. S., & Richardson, J. R. (2020) · The Journal of Comparative Neurology · doi:10.1002/cne.25089 · Cited by 14
“Elevated in AD patients, AGE products act as a mediator of inflammation and vascular dysfunction, by depositing in the vessel wall and forming crosslinks with collagen that lead to vascular stiffness (Hughes et al., 2015; Srikanth et al., 2011).”
BackgroundAlghamdi, A., Forbes, S., Birch, D. J. S., Vyshemirsky, V., & Rolinski, O. J. (2021) · Archives of Biochemistry and Biophysics · doi:10.1016/j.abb.2021.108886 · Cited by 13
Tissue expression of glycated apolipoprotein B in colorectal adenoma and cancer.
Reddavide, R., Misciagna, G., Caruso, M. G., Notarnicola, M., Armentano, R., Caruso, M. L., Pirrelli, M., & Valentini, A. M. (2011) · PubMed · Cited by 12
Lower expression level of two RAGE alternative splicing isoforms in Alzheimer’s disease
Zhu, H., & Ding, Q. (2015) · Neuroscience Letters · doi:10.1016/j.neulet.2015.04.032 · Cited by 12
Blood–Brain Barrier Transport of Alzheimer’s Amyloid β-Peptide
Nelson, A. R., Sagare, A. P., & Zloković, B. V. (2016) · Elsevier eBooks · doi:10.1016/b978-0-12-802173-6.00009-5 · Cited by 12
Watanabe, M., Toyomura, T., Wake, H., Liu, K., Teshigawara, K., Takahashi, H. K., Nishibori, M., & Mori, S. (2017) · Molecular and Cellular Biochemistry · doi:10.1007/s11010-017-3045-6 · Cited by 12
Jung, E., Kang, W. S., Jo, K., & Kim, J. (2019) · Journal of Diabetes Research · doi:10.1155/2019/4058280 · Cited by 12
Cerebrospinal fluid oxidative stress markers in Alzheimer's disease
Sakakibara, R., & Kawai, T. (2020) · Neurology and Clinical Neuroscience · doi:10.1111/ncn3.12413 · Cited by 12
Swami, P., O’Connell, K. A., Thiyagarajan, S., Crawford, A. J., Patil, P. P., Radhakrishnan, P., Shin, S. C., Caffrey, T. C., Grunkemeyer, J. A., Neville, T. L. L., et al. (2021) · Biomolecules · doi:10.3390/biom11040526 · Cited by 12
Babri, S., Amani, M., Mohaddes, G., Alihemmati, A., & Ebrahimi, H. (2012) · Neurophysiology · doi:10.1007/s11062-012-9309-6 · Cited by 12
Chen, Z., Yang, J., Fu, Y., Wan, Y., Liu, W., Wang, T., Fu, X., Liu, W., & Wei, C. (2024) · Journal of Food Science · doi:10.1111/1750-3841.17295 · Cited by 11
Influences of periodontitis on hippocampal inflammation, oxidative stress, and apoptosis in rats
Köse, O., Altın, A., Bayrakdar, S. K., Bostan, S. A., Mercantepe, T., Akyıldız, K., Tümkaya, L., Yılmaz, A., Köse, S., Yemenoğlu, H., et al. (2021) · Journal of Periodontal Research · doi:10.1111/jre.12929 · Cited by 11
Guo, M., Wang, J., Qi, H., Liu, F., Yao, L., Zhang, S., & Li, K. (2016) · Neuroscience Letters · doi:10.1016/j.neulet.2016.01.043 · Cited by 11
Enhanced carbonyl stress and disrupted white matter integrity in schizophrenia
Son, S., Arai, M., Miyata, J., Toriumi, K., Mizuta, H., Hayashi, T., Aso, T., Itokawa, M., & Murai, T. (2020) · Schizophrenia Research · doi:10.1016/j.schres.2020.08.007 · Cited by 11
New 2,3-diaminopropionic acidinhibitors of AGE and ALE formation
Audic, N., Potier, G., & Sasaki, N. A. (2012) · Organic & Biomolecular Chemistry · doi:10.1039/c2ob27084f · Cited by 11
Lilly, L., Heiss, C. J., Maragoudakis, S. F., Braden, K. L., & Smith, S. E. (2018) · Journal of the American College of Nutrition · doi:10.1080/07315724.2018.1519404 · Cited by 11
Long-Term Memory Function Impairments following Sucrose Exposure in Juvenile versus Adult Rats
Coirini, H., Rey, M., Deniselle, M. C. G., & Kruse, M. S. (2022) · Biomedicines · doi:10.3390/biomedicines10112723 · Cited by 10
“The activation of the AGE-RAGE pathway has been strongly associated with diabetes-related complications [26] and cognitive impairments in Alzheimer’s disease [27].”
BackgroundUras, G., Li, X., Manca, A., Pantaleo, A., Bo, M., Xu, J., Allen, S., & Zhu, Z. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms232314794 · Cited by 10
Waseem, R., Khan, T., Shamsi, A., Shahid, M., Kazim, S. N., Hassan, M. I., & Islam, A. (2023) · International Journal of Biological Macromolecules · doi:10.1016/j.ijbiomac.2023.125405 · Cited by 10
Płoska, A., Cieślik, P., Siekierzycka, A., Kalinowski, L., & Wierońska, J. M. (2021) · Brain Research · doi:10.1016/j.brainres.2021.147577 · Cited by 10
Novel pathways and therapies in experimental diabetic atherosclerosis
Koulis, C., de Haan, J. B., & Allen, T. J. (2012) · Expert Review of Cardiovascular Therapy · doi:10.1586/erc.12.13 · Cited by 10
Psychology and Pathophysiological Outcomes of Eating
Takada, A., & Himmerich, H. (2021) · IntechOpen eBooks · doi:10.5772/intechopen.92917 · Cited by 10
RETRACTED: On the early toxic effect of quinolinic acid: Involvement of RAGE
Cuevas, E., Lantz, S. M., Newport, G. D., Divine, B., Wu, Q., Paule, M. G., Tobón-Velasco, J. C., Ali, S. F., & Santamarı́a, A. (2010) · Neuroscience Letters · doi:10.1016/j.neulet.2010.03.007 · Cited by 10
RetractedSuh, K. S., Chon, S., & Choi, E. M. (2018) · Journal of Applied Toxicology · doi:10.1002/jat.3620 · Cited by 10
“In the presence of transition metals and oxygen, glucose and Amadori products undergo autoxidation to form free radicals (Ahmed, 2005; Srikanth et al., 2011), which cause damage to biomolecules in the body (Styskal, Van Remmen, Richardson, & Salmon, 2012).”
BackgroundStudies on mechanism of free Nε‐(carboxymethyl)lysine‐induced toxic injury in mice
Wang, Y., Xu, H., Liu, X., Liu, L., Wu, Y., & Gong, Z. (2019) · Journal of Biochemical and Molecular Toxicology · doi:10.1002/jbt.22322 · Cited by 10
Tian, C., Ye, Z., McCoy, R. G., Pan, Y., Bi, C., Gao, S., Ma, Y., Mo, C., Yu, J., Lu, T., et al. (2024) · Frontiers in Neuroscience · doi:10.3389/fnins.2023.1335500 · Cited by 10
“Some study have confirmed that AGEs formed during prolonged hyperglycemia can accumulate in brain tissues and contribute to the pathogenesis of neurodegenerative diseases (Dei et al., 2002; Srikanth et al., 2011).”
BackgroundVenuti, M. T., Roda, E., Brandalise, F., Sarkar, M., Cappelletti, M., Speciani, A. F., Soffientini, I., Priori, E. C., Giammello, F., Ratto, D., et al. (2025) · Frontiers in Physiology · doi:10.3389/fphys.2025.1455434 · Cited by 11
Qiu, Z.-K., Zhou, B.-X., Pang, J., Zeng, W.-Q., Wu, H.-B., & Yang, F. (2023) · Metabolic Brain Disease · doi:10.1007/s11011-023-01179-6 · Cited by 13
Santoro, T., de Azevedo, C. T., Silva, P., Martins, M. A., & Carvalho, V. F. (2018) · Journal of Leukocyte Biology · doi:10.1002/jlb.3a0917-364rr · Cited by 9
Leitzen, S., Vogel, M., Engels, A., Zapf, T., & Brandl, M. (2021) · PLoS ONE · doi:10.1371/journal.pone.0253811 · Cited by 9
“Furthermore, reactive amino acid side chains of proteins may react with GDPs and form so-called AGEs (advanced glycation end products) [1, 7], which are being investigated in the context of Alzheimer’s disease [14], cardiovascular disease, and stroke [15, 16].”
BackgroundThe whole‐brain voxel‐based morphometry study in early stage of T2DM patients
He, Y., Li, L., & Liu, J. (2022) · Brain and Behavior · doi:10.1002/brb3.2497 · Cited by 9
Jang, M., Lee, H., Seo, E. U., & Kim, H. N. (2025) · Biomaterials · doi:10.1016/j.biomaterials.2025.123504 · Cited by 8
Targeting the awry Aβ pathway in Alzheimer’s disease: hype and hurdles
Al-Kuraishy, H. M., Sulaiman, G. M., Al-Gareeb, A. I., Mohammed, H. A., Albuhadily, A. K., & Abomughaid, M. M. (2025) · Inflammopharmacology · doi:10.1007/s10787-025-01983-9 · Cited by 8
“Furthermore, RAGE can increase the neurotoxicity of Aβ through activation of microglia and the release of pro-inflammatory cytokines (Srikanth et al. 2011).”
Hong, X., Chen, T., Liu, Y., Li, J., Huang, D., Ye, K., Liao, W., Wang, Y., Liu, M., & Luan, P. (2025) · Ageing Research Reviews · doi:10.1016/j.arr.2025.102669 · Cited by 9
Ferretti, G., Neri, D., & Bacchetti, T. (2014) · Food and Nutrition Sciences · doi:10.4236/fns.2014.516170 · Cited by 8
“Recent studies have also shown that some fruit phenolics inhibit the formation of advanced glycation end products (AGEs) [5]-[10], whose formation and accumulation exert a pathophysiological role in patients with diabetes, renal and neurodegenerative disease as well as some types of cancer [11] [12].”
BackgroundThe Effect of Glycation Stress on Skeletal Muscle
Egawa, T., Kido, K., Yokokawa, T., Fujibayashi, M., Goto, K., & Hayashi, T. (2021) · IntechOpen eBooks · doi:10.5772/intechopen.97769 · Cited by 8
Patil, N. A., Kelkar, A., & Sivaram, A. (2022) · BioNanoScience · doi:10.1007/s12668-022-00954-6 · Cited by 8
“Thus AGE-driven extracellular amyloid plaques and intracellular tau neurofibrillary tangles build up in the neurons disrupting the structure of the neurons and widening the synaptic cleft, finally leading to loss of communication and function of the neurons [26].”
BackgroundCharacterization of dehydroascorbate‐mediated modification of glutaredoxin by mass spectrometry
Flandrin, A., Allouche, S., Rolland, Y., McDuff, F., Wagner, J. R., & Klarskov, K. (2015) · Journal of Mass Spectrometry · doi:10.1002/jms.3706 · Cited by 8
Liu, C., Wang, R., Dong, M., Gao, X.-R., & Feng, Y. (2014) · PubMed · Cited by 8
Tasca, K. I., Caleffi, J. T., Corrêa, C. R., Gatto, M., de Camargo, C. C., Mendes, M. B., Golim, M. D. A., Biasin, M., & de Souza, L. D. R. (2016) · Mediators of Inflammation · doi:10.1155/2016/2909576 · Cited by 8
“Because of the current ever-earlier recommendations to start cART and its prolonged use, these and other markers should be investigated in order to monitor and postpone the appearance of non-AIDS comorbidities in PLWHA.”
BackgroundAdvanced Glycation End Products in Chinese Medicine Mediated Aging Diseases: A Review
Zhang, W., Zhao, T., Zhao, Y., Gui, D., & Xu, Y. (2019) · Current Vascular Pharmacology · doi:10.2174/1570161117666190507112157 · Cited by 8
Babri, S., Amani, M., Mohaddes, G., Alihemmati, A., & Ebrahimi, H. (2012) · Neurophysiology · doi:10.1007/s11062-012-9328-3 · Cited by 8
Ali, M. Y., Jung, H. A., Jannat, S., & Choi, J. S. (2019) · Archives of Pharmacal Research · doi:10.1007/s12272-019-01113-4 · Cited by 8
Mikuła, E., & Malecka, K. (2023) · Coatings · doi:10.3390/coatings13020235 · Cited by 7
Neuropathological links between T2DM and LOAD: systematic review and meta-analysis
Lemche, E., Hortobágyi, T., Kiecker, C. M., & Turkheimer, F. (2025) · Physiological Reviews · doi:10.1152/physrev.00040.2024 · Cited by 9
The Association of -429T>C and -374T>A Polymorphisms in the RAGE Gene with Polycystic Ovary Syndrome
Park, J., Li, L., Choi, J.-W., & Baek, K. (2016) · International Journal of Medical Sciences · doi:10.7150/ijms.15389 · Cited by 7
RAGE Exacerbate Amyloid Beta (Aβ) Induced Alzheimer Pathology: A Systemic Overview
Akhter, F., Akhter, A., Kesari, K. K., Javed, R., Ruokolainen, J., & Vuorinen, T. (2019) · Environmental science and engineering · doi:10.1007/978-3-319-96511-6_9 · Cited by 7
Development of Disposable Single-Use Biosensor for Fructosyl Valine and Glycated Hemoglobin A1c
Liu, S. T. H., Leng, J., & Aquino, T. C. (2019) · Journal of Sensor Technology · doi:10.4236/jst.2019.94005 · Cited by 7
“In addition to diabetes, AGEs have been implicated in Alzheimer’s Disease [3], cardiovascular disease [4], and stroke [5].”
BackgroundWang, R., Xu, Z., Li, Y., Li, W., Gao, X.-R., Liu, C., & Liu, C. (2021) · Journal of Functional Foods · doi:10.1016/j.jff.2021.104644 · Cited by 7
Wang, G., Wang, X., Zheng, X., Sun, S., Zhao, J., Ying, L., & Mao, Y. (2022) · Neuroscience Research · doi:10.1016/j.neures.2022.08.005 · Cited by 7
de Fonseca, F. R., Medina-Paz, F., Sapozhnikov, M., Hurtado-Guerrero, I., Rubio, L., Martín‐de‐las‐Heras, S., Requena-Ocaña, N., Flores-López, M., Fernández‐Arjona, M. D. M., Rivera, P., et al. (2024) · Toxics · doi:10.3390/toxics12030190 · Cited by 7
“RAGE is a member of the immunoglobulin superfamily and a type I transmembrane protein that binds to AGEs, HMGB1, lipopolysaccharides, S100, and amyloid beta, among others [17,18].”
BackgroundZborowska, M., Sulima, M., Marszałek, I., Wysłouch‐Cieszyńska, A., Radecka, H., & Radecki, J. (2014) · Analytical Letters · doi:10.1080/00032719.2013.867501 · Cited by 7
“Amyloid-beta peptide is the main component of senile plaques typical of Alzheimer’s diseased brains (Finder et al. 2010; Srikanth et al. 2011).”
BackgroundSahebi, U., & Divsalar, A. (2016) · Journal of the Iranian Chemical Society · doi:10.1007/s13738-016-0917-8 · Cited by 7
Sharman, M. J., Verdile, G., Kirubakaran, S., & Münch, G. W. (2019) · Wiley eBooks · doi:10.1002/9781119356752.ch8 · Cited by 8
Self-citationSreekumar, P. G., Nam, M., Hong, E., Kannan, R., & Nagaraj, R. H. (2025) · Investigative Ophthalmology & Visual Science · doi:10.1167/iovs.66.6.30 · Cited by 6
“15,18 19–24 Polymorphisms in the RAGE gene (rs1800624 and rs1800625) have been linked to an increased susceptibility to early and exudative age-related macular degeneration (AMD).”
Singh, K., Gupta, J. K., Sethi, P., Mathew, S., Bhatt, A., Sharma, M. C., Saha, S., Khan, S., & Kumar, S. (2024) · Current Topics in Medicinal Chemistry · doi:10.2174/0115680266305736240725052825 · Cited by 6
Characterization and cytological effects of a novel glycated gelatine substrate
Boonkaew, B., Tompkins, K. A., Manokawinchoke, J., Pavasant, P., & Supaphol, P. (2014) · Biomedical Materials · doi:10.1088/1748-6041/9/2/025001 · Cited by 6
Yang, Y., Nourian, Z., Li, M., Sun, Z., Zhang, L., Davis, M. J., Meininger, G. A., Wu, J., Braun, A. P., & Hill, M. A. (2022) · Frontiers in Physiology · doi:10.3389/fphys.2022.871968 · Cited by 6
“Rat lung total RNA was also purified as a positive control for RAGE mRNA expression (Srikanth et al., 2011).”
MethodYang, J., Lin, M., Zhang, M., Wang, Z., Lin, H., Yu, Y., Zheng, Q., Chen, X., Wu, Y., Yao, Q., et al. (2023) · Genetics Research · doi:10.1155/2023/7129325 · Cited by 5
Recent advances in nanotechnology for combating Alzheimer's disease
Hu, C., Wu, B., Wu, Y., Shi, M., Ma, J., Gao, H., & Zhang, J. (2023) · Materials Chemistry Frontiers · doi:10.1039/d3qm00493g · Cited by 7
Cytotoxic role of advanced glycation end-products in PC12 cells treated with β-amyloid peptide
Yan, F., HAN, G.-L., & WU, G.-J. (2013) · Molecular Medicine Reports · doi:10.3892/mmr.2013.1545 · Cited by 6
Not only a bad guy: potential proneurogenic role of the RAGE/NF-κB axis in Alzheimer's disease brain
Grilli, M., & Bortolotto, V. (2016) · Neural Regeneration Research · doi:10.4103/1673-5374.197130 · Cited by 6
“This concept is in agreement with previous work showing that infusion of picomolar concentrations of Aβ oligomers can indeed enhance long term potentiation in hippocampal slices and significantly improve spatial long-term hippocampal memory (Srikanth et al., 2011).”
The Chemistry of Advanced Glycation End-products
Torres, N. M. P. O., Xavier, J. A., Goulart, M. O. F., Alves, R. B., & de Freitas, R. P. (2018) · Revista Virtual de Química · doi:10.21577/1984-6835.20180029 · Cited by 6
Lee, C. H., Kim, K. W., Lee, D.-H., Lee, S. M., & Kim, S. Y. (2021) · BMC Neuroscience · doi:10.1186/s12868-021-00642-3 · Cited by 6
“Background The receptor for advanced glycation end-products (RAGE) is a transmembrane receptor of the immunoglobulin superfamily and can bind to multiple ligands, including advanced glycation end-products (AGEs) and β-amyloid peptide [3, 27].”
BackgroundDiabetes and cognitive dysfunction
Kim, B., Sims‐Robinson, C., Sakowski, S. A., & Feldman, E. L. (2022) · Elsevier eBooks · doi:10.1016/b978-0-323-85654-6.00027-7 · Cited by 8
Sex Differences in Obesity-Induced Inflammation
Terrazas, S., Brashear, L., Escoto, A.-K., Lynch, S. E., Slaughter, D., Xavier, N., Estes, N. R., & Giordano‐Mooga, S. (2019) · IntechOpen eBooks · doi:10.5772/intechopen.84941 · Cited by 6
“Advanced glycation end products, or AGEs, are markers of carbonyl stress due to oxidative stress, and their formation is irreversible and leads to protein deposits and amyloidosis [92].”
BackgroundInfluentialMurakami, Y., Fujino, T., Hasegawa, T., Kurachi, R., Miura, A., Daikoh, T., Usui, T., Hayase, F., & Watanabe, H. (2018) · Bioscience Biotechnology and Biochemistry · doi:10.1080/09168451.2017.1422971 · Cited by 6
“There is accumulating evidence that the AGEsRAGE interaction is implicated in neurodegenerative diseases as well as diabetic complications [6].”
BackgroundUpadhyay, R. K., Pradhan, D., Parshad, R. D., & Roy, P. (2024) · Communications in Nonlinear Science and Numerical Simulation · doi:10.1016/j.cnsns.2024.108396 · Cited by 5
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
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