Cited by 526Advanced Glycation End Products researchAlzheimer's disease research and treatmentsDementia and Cognitive Impairment Research

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Advanced glycation endproducts and their receptor RAGE in Alzheimer's disease

Srikanth, Velandai, Maczurek, Annette, Phan, Thanh, Steele, Megan, Westcott, Bernadette, Juskiw, Damian, Münch, Gerald·2011·Neurobiology of Aging

DOI 10.1016/j.neurobiolaging.2009.04.016

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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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Self-citation
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“…ligands: LPS (binding to Toll like receptor 4 (Beutler, 2002), interferon-γ (IFN-γ, binding to the interferon-γ receptor) (Griggs et al., 1992) or AGEs (binding to receptor for AGEs) (Srikanth et al., 2011) in the presence of increasing concentrations of (hydrogen peroxide detoxifying) catalase.”
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l ‐Theanine Ameliorates d ‐Galactose‐Induced Brain Damage in Rats via Inhibiting AGE Formation and Regulating Sirtuin1 and BDNF Signaling Pathways
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Self-citation

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)
ORCID: Srikanth, Velandai
Phan, Thanh
Steele, Megan
Münch, Gerald
Venue: Neurobiology of Aging
Publisher: Elsevier BV
Published: 2011-05
Volume: 32
Issue: 5
Pages: 763-777
ISSN: 0197-4580 (ISSN-L)
DOI: 10.1016/j.neurobiolaging.2009.04.016
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: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
www.elsevier.com/legal/tdmrep-license (tdm)
doi.org/10.15223/policy-017 (stm-asf)
doi.org/10.15223/policy-037 (stm-asf)
doi.org/10.15223/policy-012 (stm-asf)
doi.org/10.15223/policy-029 (stm-asf)
doi.org/10.15223/policy-004 (stm-asf)
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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Advanced glycation endproducts and their receptor RAGE in Alzheimer's disease

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