D-β-Hydroxybutyrate rescues mitochondrial respiration and mitigates features of Parkinson disease
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Issue Date
2003-09-15Author
Tieu, Kim
Perier, Celine
Caspersen, Casper
Tiesmann, Peter
Wu, Du-Chu
Yan, Shirley ShiDu
Naini, Ali
Vila, Miquel
Jackson-Lewis, Vernice
Ramasamy, Ravichandran
Przedborski, Serge
Publisher
American Society for Clinical Investigation
Type
Article
Article Version
Scholarly/refereed, publisher version
Metadata
Show full item recordAbstract
Parkinson disease (PD) is a neurodegenerative disorder characterized by a loss of the nigrostriatal dopaminergic neurons accompanied by a deficit in mitochondrial respiration. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) is a neurotoxin that causes dopaminergic neurodegeneration and a mitochondrial deficit reminiscent of PD. Here we show that the infusion of the ketone body D-β-hydroxybutyrate (DβHB) in mice confers partial protection against dopaminergic neurodegeneration and motor deficits induced by MPTP. These effects appear to be mediated by a complex II–dependent mechanism that leads to improved mitochondrial respiration and ATP production. Because of the safety record of ketone bodies in the treatment of epilepsy and their ability to penetrate the blood-brain barrier, DβHB may be a novel neuroprotective therapy for PD.
Description
This is the published version. Copyright 2003 : American Society for Clinical Investigation.
Collections
- Pharmacy Scholarly Works [293]
Citation
Tieu, Kim, Celine Perier, Casper Caspersen, Peter Teismann, Du-Chu Wu, Shi-Du Yan, Ali Naini, Miquel Vila, Vernice Jackson-Lewis, Ravichandran Ramasamy, and Serge Przedborski. "D-β-Hydroxybutyrate Rescues Mitochondrial Respiration and Mitigates Features of Parkinson Disease." Journal of Clinical Investigation J. Clin. Invest. 112.6 (2003): 892-901. http://dx.doi.org/10.1172/JCI18797.
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