Coenzyme Q10 Long-Term Supplementation May Result in Withdrawal Effect in Myocardium
Authors: Meredith Spindler, M Flint Beal, Claire Henchcliffe
Published Date November 2009 , Volume 2009:5 Pages 597 - 610 DOI 10.2147/NDT.S5212
Meredith Spindler, M Flint Beal, Claire Henchcliffe
Department of Neurology, 2Department of Neuroscience, Weill Medical College of Cornell University, New York, NY, USA
Coenzyme Q10 (CoQ10) is an essential co-factor in the mitochondrial respiratory chain, and as a dietary supplement it has recently gained attention for its potential role in the treatment of neurodegenerative disease. Evidence for mitochondrial dysfunction in neurodegenerative disorders derives from animal models, studies of mitochondria from patients, identification of genetic defects in patients with neurodegenerative disease, and measurements of markers of oxidative stress.
Studies of in vitro models of neuronal toxicity and animal models of neurodegenerative disorders have demonstrated potential neuroprotective effects of CoQ10. With this data in mind, several clinical trials of CoQ10 have been performed in Parkinson’s disease and atypical Parkinson’s syndromes, Huntington’s disease, Alzheimer disease, Friedreich’s ataxia, and amyotrophic lateral sclerosis, with equivocal findings.
CoQ10 is widely available in multiple formulations and is very well tolerated with minimal adverse effects, making it an attractive potential therapy. Phase III trials of high-dose CoQ10 in large sample sizes are needed to further ascertain the effects of CoQ10 in neurodegenerative diseases.