ME/CFS AUSTRALIA (SA) INC
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CoQ10 depletion implicated in Fibromyalgia, ME/CFS, and Parkinson's
Friday 21 June 2013
Coenzyme Q10 Depletion in Medical and Neuropsychiatric Disorders: Potential Repercussions and Therapeutic Implications.
Coenzyme Q10 (CoQ10) is an antioxidant, a membrane stabilizer, and a vital cofactor in the mitochondrial electron transport chain, enabling the generation of adenosine triphosphate. It additionally regulates gene expression and apoptosis; is an essential cofactor of uncoupling proteins; and has anti-inflammatory, redox modulatory, and neuroprotective effects.
This paper reviews the known physiological role of CoQ10 in cellular metabolism, cell death, differentiation and gene regulation, and examines the potential repercussions of CoQ10 depletion including its role in illnesses such as Parkinson's disease, depression, myalgic encephalomyelitis/chronic fatigue syndrome, and fibromyalgia.
CoQ10 depletion may play a role in the pathophysiology of these disorders by modulating cellular processes including hydrogen peroxide formation, gene regulation, cytoprotection, bioenegetic performance, and regulation of cellular metabolism.
The evidence base for the effectiveness of treatment with CoQ10 may be explained via its ability to ameliorate oxidative stress and protect mitochondria.
Source: Molecular Neurobiology, June 13, 2013. By Gerwyn Morris, George Anderson, Michael Berk and Michael Maes. Tir Na Nog, Bryn Road seaside 87, Llanelli, SA152LW, Wales, UK.
The above originally appeared here.
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