Causes of oxidative stress in Alzheimer disease
Open accessAbstract
Oxidative stress is one of the earliest events of Alzheimer disease (AD), with implications as an important mediator in the onset, progression and pathogenesis of the disease. The generation of reactive oxygen species (ROS) and its consequent cellular damage/response contributes to much of the hallmark AD pathology seen in susceptible neurons. The sources of ROS-mediated damage appear to be multi-faceted in AD, with interactions between abnormal mitochondria, redox transition metals, and other factors. In this review, we provide an overview of these potential causes of oxidative stress in AD.
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Metal ions promote Aβ aggregation and formation of reactive oxygen species and lead to oxidative stress.
“For example, it was shown that that metal ions promote Aβ aggregation,16,17 as well as formation of reactive oxygen species (ROS) and lead to oxidative stress.18–20”
From The effect of Cu2+ and Zn2+ on the Aβ42 peptide aggregation and cellular toxicity (2013) · cites this paper as [19]
These metal ions lead to formation of reactive oxygen species (ROS) and oxidative stress.
“as well as lead to formation of reactive oxygen species (ROS) and oxidative stress.3,26–31,33–36”
From Bifunctional Compounds for Controlling Metal-Mediated Aggregation of the Aβ<sub>42</sub>Peptide (2012) · cites this paper as [34]
Copper, iron, and zinc ions affect Aβ aggregation and lead to formation of reactive oxygen species.
“These metal ions have been shown to affect Aβ aggregation, as well as lead to the formation of reactive oxygen species (ROS).12−16”
From Small Bifunctional Chelators That Do Not Disaggregate Amyloid β Fibrils Exhibit Reduced Cellular Toxicity (2014) · cites this paper as [15]
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- Authors
- Zhu, X., Su, B., Wang, X., Smith, M. A., & Perry, G.
- Affiliations
- Case Western Reserve University (US)
- The University of Texas at San Antonio (US)
- Corresponding author
- Perry, G.
- Venue
- Cellular and Molecular Life Sciences
- Published
- 2007-07-02
- Volume
- 64
- Issue
- 17
- Pages
- 2202-2210
- ISSN
- 1420-682X (ISSN-L)
- 1420-9071
- PMC
- PMC11136009
- OpenAlex
- W2064625375
- Cited by
- 336
- References
- 117
- Citations by year
- 2026: 3 · 2025: 4 · 2024: 6 · 2023: 12 · 2022: 10 · 2021: 9 · 2020: 17 · 2019: 12 · 2018: 16 · 2017: 16 · 2016: 10 · 2015: 26 · 2014: 28 · 2013: 11 · 2012: 38
- FWCI
- 20.92
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Cellular and Molecular Life Sciences (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Keywords
- oxidative stress, Alzheimer's disease, reactive oxygen species, mitochondrial dysfunction, neurodegeneration, neuronal injury, pathogenesis
- MeSH terms
- Alzheimer Disease, Astrocytes, Copper, Glycosylation, Humans, Iron, Mitochondria, Oxidation-Reduction, Glycation End Products, Advanced, Reactive Oxygen Species, Microglia, Oxidative Stress
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