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

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

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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Crossref · 10.1016/j.neurobiolaging.2009.04.016

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Research works printed but not linked: 2

  1. 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
  2. Yan, 1996, RAGE and amyloid-beta peptide neurotoxicity in Alzheimer's disease, Nature, 382, 685, 10.1038/382685a0 · DOI · Paper page

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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)
ORCID
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
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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