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Potential for creatine and other therapies targeting cellular energy dysfunction in neurological disorders
Abstract
Substantial evidence indicates that bioenergetic dysfunction plays either a primary or secondary role in the pathophysiology of cell death in neurodegenerative and neuromuscular disorders, and even in normal aging. Agents that ameliorate bioenergetic defects may therefore be useful in therapy. Creatine, which increases muscle and brain phosphocreatine concentrations, and may inhibit the activation of the mitochondrial permeability transition, protects against neuronal degeneration in transgenic murine models of amyotrophic lateral sclerosis and Huntington's disease and in chemically mediated neurotoxicity. Initial studies of creatine use in humans appear promising; however, further long‐term, well‐designed trials are needed. Coenzyme Q 10 , Gingko biloba , nicotinamide, riboflavin, carnitine, lipoic acid, and dichloroacetate are other agents which may have beneficial effects on energy metabolism, but the preclinical and clinical evidence for efficacy in neurological diseases remains limited. These compounds are widely used as dietary supplements; however, they must be subjected to rigorous evaluation through randomized, double‐blinded trials to establish efficacy, cost‐effectiveness and safety in neurological disorders.
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“At the cellular level, there is evidence for similar final common pathways of oxidative stress, mitochondrial dysfunction, stem cell depletion, reduced protein synthesis, apoptosis, and inflammation [44].”
From Creatine monohydrate supplementation for older adults and clinical populations (2025) · cites this paper as [44]
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“it is likely that the potential benefits of CrM will be best realized when it is a part of a multi-ingredient supplement strategy that targets the final common pathways of muscle pathology in patients with myopathies [44]”
From Creatine monohydrate supplementation for older adults and clinical populations (2025) · cites this paper as [44]
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Metadata
- Authors
- Tarnopolsky, M. A., & Beal, M. F.
- Venue
- Annals of Neurology
- Publisher
- Wiley
- Published
- 2001-04-26
- Volume
- 49
- Issue
- 5
- Pages
- 561-574
- ISSN
- 0364-5134
- 1531-8249
- Cited by
- 195
- References
- 29
- Language
- en
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