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Bioenergetic approaches for neuroprotection in Parkinson's disease.
Ann Neurol. 2003; 53 Suppl 3:S39-47; discussion S47-8.AN

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.

Authors+Show Affiliations

Department of Neurology and Neuroscience, Weill Medical College of Cornell University, New York Presbyterian Hospital, New York, NY, USA. fbeal@mail.med.cornell.edu

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, Non-P.H.S.
Research Support, U.S. Gov't, P.H.S.
Review

Language

eng

PubMed ID

12666097

Citation

Beal, M Flint. "Bioenergetic Approaches for Neuroprotection in Parkinson's Disease." Annals of Neurology, vol. 53 Suppl 3, 2003, pp. S39-47; discussion S47-8.
Beal MF. Bioenergetic approaches for neuroprotection in Parkinson's disease. Ann Neurol. 2003;53 Suppl 3:S39-47; discussion S47-8.
Beal, M. F. (2003). Bioenergetic approaches for neuroprotection in Parkinson's disease. Annals of Neurology, 53 Suppl 3, S39-47; discussion S47-8.
Beal MF. Bioenergetic Approaches for Neuroprotection in Parkinson's Disease. Ann Neurol. 2003;53 Suppl 3:S39-47; discussion S47-8. PubMed PMID: 12666097.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Bioenergetic approaches for neuroprotection in Parkinson's disease. A1 - Beal,M Flint, PY - 2003/4/1/pubmed PY - 2003/4/26/medline PY - 2003/4/1/entrez SP - S39-47; discussion S47-8 JF - Annals of neurology JO - Ann Neurol VL - 53 Suppl 3 N2 - 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. SN - 0364-5134 UR - https://www.unboundmedicine.com/medline/citation/12666097/Bioenergetic_approaches_for_neuroprotection_in_Parkinson's_disease_ L2 - https://doi.org/10.1002/ana.10479 DB - PRIME DP - Unbound Medicine ER -