Abstract
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.
Original language | English (US) |
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Pages (from-to) | 2202-2210 |
Number of pages | 9 |
Journal | Cellular and Molecular Life Sciences |
Volume | 64 |
Issue number | 17 |
DOIs | |
State | Published - Sep 2007 |
Externally published | Yes |
Keywords
- Alzheimer disease
- Amyloid-β
- Antioxidant
- Iron
- Metals
- Mitochondria
- Oxidative stress
- Pathogenesis
- Phosphorylation
- Reactive oxygen species
- Tau
ASJC Scopus subject areas
- Molecular Medicine
- Molecular Biology
- Pharmacology
- Cellular and Molecular Neuroscience
- Cell Biology