Cited by 113Advanced Glycation End Products researchAlzheimer's disease research and treatmentsBiochemical effects in animals

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AGES in brain ageing: AGE-inhibitors as neuroprotective and anti-dementia drugs?

Dukic-Stefanovic, Sladjana, Schinzel, Reinhard, Riederer, Peter, Münch*, Gerald·2001·Biogerontology

DOI 10.1023/a:1010052800347

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Abstract

In Alzheimer's disease, age-related cellular changes such as compromised energy production and increased radical formation are worsened by the presence of AGEs as additional, AD specific stress factors. Intracellular AGEs (most likely derived from methylglyoxal) crosslink cytoskeletal proteins and render them insoluble. These aggregates inhibit cellular functions including transport processes and contribute to neuronal dysfunction and death. Extracellular AGEs, which accumulate in ageing tissue (but most prominently on long-lived protein deposits like the senile plaques) exert chronic oxidative stress on neurons. In addition, they activate glial cells to produce free radicals (superoxide and NO) and neurotoxic cytokines such as TNF-alpha. Drugs, which inhibit the formation of AGEs by specific chemical mechanisms (AGE-inhibitors), including aminoguanidine, carnosine, tenilsetam, OPB-9195 and pyridoxamine, attenuate the development of (AGE-mediated) diabetic complications. Assuming that 'carbonyl stress' contributes significantly to the progression of Alzheimer's disease, AGE-inhibitors might also become interesting novel therapeutic drugs for treatment of AD.

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Czech C, Monning U, Tienari PJ, Hartmann T, Masters C, Beyreuther K and Forstl H (1993) Apolipoprotein-e-sigma-4 allele and alzheimers disease. Lancet 342: 1309-1310
Khalifah RG, Baynes JW and Hudson BG (1999) Amadorins: Novel post-Amadori inhibitors of advanced glycation reactions. Biochem Biophys Res Commun 257: 251-258 · DOI

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Sterile inflammation: sensing and reacting to damage
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Authors: Dukic-Stefanovic, S., Schinzel, R., Riederer, P., & Münch*, G.
Affiliations: University of Würzburg (DE)
ORCID: Schinzel, Reinhard
Riederer, Peter
Venue: Biogerontology
Publisher: Springer Science and Business Media LLC
Published: 2001-03
Volume: 2
Issue: 1
Pages: 19-34
ISSN: 1389-5729 (ISSN-L)
1573-6768
DOI: 10.1023/a:1010052800347
OpenAlex: W17453112
Cited by: 113
References: 83
Citations by year: 2024: 1 · 2023: 2 · 2022: 2 · 2021: 3 · 2020: 4 · 2019: 2 · 2018: 3 · 2017: 4 · 2016: 5 · 2015: 1 · 2014: 9 · 2013: 4 · 2012: 4
FWCI: 0.54
Type: journal article
Language: en
Open access: closed
Licence: www.springernature.com/gp/researchers/text-and-data-mining (tdm)
www.springernature.com/gp/researchers/text-and-data-mining (vor)
Locations: Biogerontology (publishedVersion)
PubMed (publishedVersion)
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 › Physiology (medical) › Biochemical effects in animals
Keywords: advanced glycation end products, AGE inhibitors, Alzheimer's disease, neuroprotection, anti-dementia drugs, methylglyoxal, carbonyl stress, oxidative stress, amyloid plaques, aminoguanidine, carnosine, pyridoxamine, glial activation, neuronal dysfunction, brain aging
MeSH terms: Aging, Alzheimer Disease, Animals, Brain, Dementia, Humans, Signal Transduction, Glycation End Products, Advanced, Neuroprotective Agents

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AGES in brain ageing: AGE-inhibitors as neuroprotective and anti-dementia drugs?

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