The DOI matches its Crossref record; 15 of the 15 references it cites were found in a registry or an index.
Aging, energy, and oxidative stress in neurodegenerative diseases
Abstract
The etiology of neurodegenerative diseases remains enigmatic; however, evidence for defects in energy metabolism, excitotoxicity, and for oxidative damage is increasingly compelling. It is likely that there is a complex interplay between these mechanisms. A defect in energy metabolism may lead to neuronal depolarization, activation of N‐methyl‐D‐aspartate excitatory amino acid‐receptors, and increases in intracellular calcium, which are buffered by mitochondria. Mitochondria are the major intracellular source of free radicals, and increased mitochondrial calcium concentrations enhance free radical generation. Mitochondrial DNA is particularly susceptible to oxidative stress, and there is evidence of age‐dependent damage and deterioration of respiratory enzyme activities with normal aging. This may contribute to the delayed onset and age dependence of neurodegenerative diseases. There is evidence for increased oxidative damage to macromolecules in amyotrophic lateral sclerosis, Huntington's disease, Parkinson's disease, and Alzheimer's disease. Potential therapeutic approaches include glutamate release inhibitors, excitatory amino acid antagonists, strategies to improve mitochondrial function, free radical scavengers, and trophic factors. All of these approaches appear promising in experimental studies and are now being applied to human studies.
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Cites
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Oxidative damage to mitochondrial DNA is increased in Alzheimer’s disease
Mecocci, P., MacGarvey, U., & Beal, M. F. (1994) · Annals of Neurology · doi:10.1002/ana.410360510 · Cited by 1,037
Self-citationMitochondrial DNA deletions in human brain: regional variability and increase with advanced age
Corral-Debrinski, M., Horton, T., Lott, M. T., Shoffner, J. M., Flint Beal, M., & Wallace, D. C. (1992) · Nature Genetics · doi:10.1038/ng1292-324 · Cited by 890
Oxidative damage to mitochondrial DNA shows marked age-dependent increases in human brain
Mecocci, P., MacGarvey, U., Kaufman, A. E., Koontz, D., Shoffner, J. M., Wallace, D. C., & Beal, M. F. (1993) · Annals of Neurology · doi:10.1002/ana.410340416 · Cited by 757
Cytochrome oxidase deficiency in Alzheimer’s disease
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Alternative excitotoxic hypotheses
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Brain cytochrome oxidase in Alzheimer's disease
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Autopsy Samples of Alzheimer's Cortex Show Increased Peroxidation In Vitro
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Cited by
The Free Radical Theory of Aging Matures
BECKMAN, K. B., & AMES, B. N. (1998) · Physiological Reviews · doi:10.1152/physrev.1998.78.2.547 · Cited by 3,879
Plasma Homocysteine as a Risk Factor for Dementia and Alzheimer's Disease
Seshadri, S., Beiser, A., Selhub, J., Jacques, P. F., Rosenberg, I. H., D'Agostino, R. B., Wilson, P. W. F., & Wolf, P. A. (2002) · New England Journal of Medicine · doi:10.1056/nejmoa011613 · Cited by 3,237
Environmentally induced oxidative stress in aquatic animals
Lushchak, V. I. (2011) · Aquatic Toxicology · doi:10.1016/j.aquatox.2010.10.006 · Cited by 2,729
Oxidative stress hypothesis in Alzheimer’s disease
Markesbery, W. R. (1997) · Free Radical Biology and Medicine · doi:10.1016/s0891-5849(96)00629-6 · Cited by 2,383
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Metadata
- Authors
- Beal, M. F.
- Venue
- Annals of Neurology
- Publisher
- Wiley
- Published
- 1995-09
- Volume
- 38
- Issue
- 3
- Pages
- 357-366
- ISSN
- 0364-5134 (ISSN-L)
- 1531-8249
- OpenAlex
- W2140075873
- Cited by
- 1,440
- References
- 15
- FWCI
- 21.91
- Type
- journal article
- Language
- en
- Open access
- closed
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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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