Oxidative stress in Alzheimer disease
Open accessAbstract
Alzheimer disease (AD) is a progressive dementia affecting a large proportion of the aging population. The histopathological changes in AD include neuronal cell death, formation of amyloid plaques and neurofibrillary tangles. There is also evidence that brain tissue in patients with AD is exposed to oxidative stress (e.g., protein oxidation, lipid oxidation, DNA oxidation and glycoxidation) during the course of the disease. Advanced glycation endproducts (AGEs) are present in amyloid plaques in AD, and its extracellular accumulation may be caused by an accelerated oxidation of glycated proteins. AGEs participate in neuronal death causing direct (chemical) and indirect (cellular) free radical production and consequently increase oxidative stress. The development of drugs for the treatment of AD that breaks the vicious cycles of oxidative stress and neurodegeneration offer new opportunities. These approaches include AGE-inhibitors, antioxidants and anti-inflammatory substances, which prevent free radical production.
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Aβ plaques facilitate a positive feedback loop of increasing oxidative stress and elevated Aβ levels, leading to neuritic dystrophy and neuronal death.
“Aβ plaques also play a role in facilitating a positive feedback loop of increasing oxidative stress and subsequently elevated Aβ levels, leading to neuritic dystrophy and culminating in neuronal death [16,17,18,19].”
From Centella Asiatica Improves Memory and Promotes Antioxidative Signaling in 5XFAD Mice (2019) · cites this paper as [17]
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Biochemical deficits and cognitive decline in brain aging: Intervention by dietary supplements
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- Authors
- Gella, A., & Durany, N.
- Affiliations
- Universitat Internacional de Catalunya (ES)
- Corresponding author
- Gella, Alejandro
- ORCID
- Gella, Alejandro
- Venue
- Cell Adhesion & Migration
- Publisher
- Informa UK Limited
- Published
- 2009-01
- Volume
- 3
- Issue
- 1
- Pages
- 88-93
- ISSN
- 1933-6918 (ISSN-L)
- 1933-6926
- PMC
- PMC2675154
- OpenAlex
- W2000446523
- Cited by
- 459
- References
- 97
- Citations by year
- 2026: 23 · 2025: 45 · 2024: 42 · 2023: 56 · 2022: 41 · 2021: 36 · 2020: 20 · 2019: 34 · 2018: 25 · 2017: 27 · 2016: 20 · 2015: 11 · 2014: 20 · 2013: 18 · 2012: 14
- FWCI
- 1.39
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Cell Adhesion & Migration (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Clinical Biochemistry › Advanced Glycation End Products research
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Keywords
- Alzheimer's disease, oxidative stress, advanced glycation end products, amyloid plaques, neurofibrillary tangles, protein oxidation, lipid peroxidation, DNA oxidation, glycoxidation, free radicals, neuronal cell death, neurodegeneration, antioxidants, anti-inflammatory agents, AGE inhibitors
- MeSH terms
- Alzheimer Disease, Animals, Glucose, Humans, Oxidation-Reduction, Glycation End Products, Advanced, Oxidative Stress, Feedback, Physiological
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