Oxidative Stress Mediated Mitochondrial and Vascular Lesions as Markers in the Pathogenesis of Alzheimer Disease
Abstract
Mitochondrial dysfunction plausibly underlies the aging-associated brain degeneration. Mitochondria play a pivotal role in cellular bioenergetics and cell-survival. Oxidative stress consequent to chronic hypoperfusion induces mitochondrial damage, which is implicated as the primary cause of cerebrovascular accidents (CVA) mediated Alzheimer's disease (AD). The mitochondrial function deteriorates with aging, and the mitochondrial damage correlates with increased intracellular production of oxidants and pro-oxidants. The prolonged oxidative stress and the resultant hypoperfusion in the brain tissues stimulate the expression of nitric oxide synthase (NOS) enzymes, which further drives the formation of reactive oxygen species (ROS) and reactive nitrogen species (RNS). The ROS and RNS collectively contributes to the dysfunction of the blood-brain barrier (BBB) and damage to the brain parenchymal cells. Delineating the molecular mechanisms of these processes may provide clues for the novel therapeutic targets for CVA and AD patients.
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Oxidative stress and mitochondrial impairment are central amplifiers of cellular injury in AD.
“Cholinergic dysfunction has long been recognized as a correlate of cognitive decline, while oxidative stress and mitochondrial impairment are increasingly appreciated as central amplifiers of cellular injury [12, 13].”
From Toward a Unified Framework in Molecular Neurobiology of Alzheimer’s Disease: Revisiting the Pathophysiological Hypotheses (2026) · cites this paper as [12]
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- Authors
- Aliev, G., Priyadarshini, M., Reddy, V., Grieg, N. H., Kaminsky, Y., Cacabelos, R., Ashraf, G., Jabir, N. R., Kamal, M. A., Nikolenko, V. N., Jr., A. A., Benberin, V., & Bachurin, S. O.
- Affiliations
- Bentham Science Publishers (United Arab Emirates) (AE)
- Venue
- Current Medicinal Chemistry
- Publisher
- Bentham Science Publishers Ltd.
- Published
- 2014-04
- Volume
- 21
- Issue
- 19
- Pages
- 2208-2217
- ISSN
- 0929-8673 (ISSN-L)
- OpenAlex
- W2135309875
- Cited by
- 138
- References
- 10
- Citations by year
- 2025: 7 · 2024: 5 · 2023: 4 · 2022: 8 · 2021: 17 · 2020: 9 · 2019: 9 · 2018: 19 · 2017: 9 · 2016: 22 · 2015: 20 · 2014: 8 · 2013: 1
- FWCI
- 7.42
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Current Medicinal Chemistry (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
- Keywords
- Alzheimer's disease, oxidative stress, mitochondrial dysfunction, stroke, hypoperfusion, nitric oxide synthase, reactive oxygen species, reactive nitrogen species, blood-brain barrier, vascular lesions, aging, neurodegeneration, therapeutic target
- MeSH terms
- Alzheimer Disease, Animals, Antioxidants, Brain, Humans, Mitochondria, Oxidative Stress
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