AGES in brain ageing: AGE-inhibitors as neuroprotective and anti-dementia drugs?
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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From Sterile inflammation: sensing and reacting to damage (2010) · cites this paper as [96]
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Self-citation
- Authors
- Dukic-Stefanovic, S., Schinzel, R., Riederer, P., & Münch*, G.
- Affiliations
- University of Würzburg (DE)
- Venue
- Biogerontology
- Published
- 2001-03
- Volume
- 2
- Issue
- 1
- Pages
- 19-34
- ISSN
- 1389-5729 (ISSN-L)
- 1573-6768
- OpenAlex
- W17453112
- Cited by
- 113
- References
- 82
- 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
- Locations
- Biogerontology (publishedVersion)
- PubMed (publishedVersion)
- 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 › Physiology › 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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