The DOI matches its Crossref record; 95 of the 97 references it cites were found in a registry or an index.
Bioenergetic approaches for neuroprotection in Parkinson's disease
Abstract
There is considerable evidence suggesting that mitochondrial dysfunction and oxidative damage may play a role in the pathogenesis of Parkinson's disease (PD). This possibility has been strengthened by recent studies in animal models, which have shown that a selective inhibitor of complex I of the electron transport gene can produce an animal model that closely mimics both the biochemical and histopathological findings of PD. Several agents are available that can modulate cellular energy metabolism and that may exert antioxidative effects. There is substantial evidence that mitochondria are a major source of free radicals within the cell. These appear to be produced at both the iron-sulfur clusters of complex I as well as the ubiquinone site. Agents that have shown to be beneficial in animal models of PD include creatine, coenzyme Q(10), Ginkgo biloba, nicotinamide, and acetyl-L-carnitine. Creatine has been shown to be effective in several animal models of neurodegenerative diseases and currently is being evaluated in early stage trials in PD. Similarly, coenzyme Q(10) is also effective in animal models and has shown promising effects both in clinical trials of PD as well as in clinical trials in Huntington's disease and Friedreich's ataxia. Many other agents show good human tolerability. These agents therefore are promising candidates for further study as neuroprotective agents in PD.
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“Creatine supplementation was found to be neuroprotective in a series of in vitro and in vivo studies101.”
From Mitochondrial Approaches for Neuroprotection (2008) · cites this paper as [101]
Citations
Cites
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Cited by
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The Role of Oxidative Stress in Parkinson's Disease
Dias, V., Junn, E., & Mouradian, M. M. (2013) · Journal of Parkinson’s Disease · doi:10.3233/jpd-130230 · Cited by 1,845
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Metadata
- Authors
- Beal, M. F.
- Affiliations
- NewYork–Presbyterian Hospital (US)
- Corresponding author
- Beal, M. Flint
- Venue
- Annals of Neurology
- Publisher
- Wiley
- Published
- 2003
- Volume
- 53
- Issue
- S3
- Pages
- S39-S48
- ISSN
- 0364-5134 (ISSN-L)
- 1531-8249
- OpenAlex
- W2102440831
- Cited by
- 236
- References
- 97
- Citations by year
- 2026: 4 · 2025: 4 · 2024: 3 · 2023: 10 · 2022: 2 · 2021: 8 · 2020: 5 · 2019: 8 · 2018: 3 · 2017: 4 · 2016: 5 · 2015: 9 · 2014: 5 · 2013: 12 · 2012: 8
- FWCI
- 2.59
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Annals of Neurology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Clinical Neurology › Parkinson's Disease Mechanisms and Treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Coenzyme Q10 studies and effects
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Keywords
- Parkinson's disease, neuroprotection, mitochondrial dysfunction, oxidative stress, mitochondrial complex I inhibition, electron transport chain, free radicals, iron-sulfur clusters, coenzyme Q10, creatine, Ginkgo biloba, nicotinamide, acetyl-L-carnitine, energy metabolism, antioxidants, Parkinson's disease model
- MeSH terms
- Acetylcarnitine, Coenzymes, Creatine, Energy Metabolism, Free Radicals, Humans, Thioctic Acid, Phytotherapy, Mitochondria, Niacinamide, Parkinson Disease, Ubiquinone, Neuroprotective Agents, Nootropic Agents, Ginkgo biloba
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