Coenzyme Q10:A Review of Its Promise as a Neuroprotectant

Abstract

Coenzyme Q10 (CoQ10) is a powerful antioxidant that buffers the potential adverse consequences of free radicals produced during oxidative phosphorylation in the inner mitochondrial membrane. Oxidative stress, resulting in glutathione loss and oxidative DNA and protein damage, has been implicated in many neurodegenerative disorders, including Alzheimer's disease, Parkinson's disease, and Huntington's disease. Experimental studies in animal models suggest that CoQ10 may protect against neuronal damage that is produced by ischemia, atherosclerosis and toxic injury. Though most have tended to be pilot studies, there are published preliminary clinical trials showing that CoQ10 may offer promise in many brain disorders. For example, a 16-month randomized, placebo-controlled pilot trial in 80 subjects with mild Parkinson's disease found significant benefits for oral CoQ10 1,200 mg/day to slow functional deterioration. However, to date, there are no published clinical trials of CoQ10 in Alzheimer's disease. Available data suggests that oral CoQ10 seems to be relatively safe and tolerated across the range of 300–2,400 mg/day. Randomized controlled trials are warranted to confirm CoQ10's safety and promise as a clinically effective neuroprotectant.

Potent induction of total cellular GSH and NQO1 as well as mitochondrial GSH by 3H-1,2-dithiole-3-thione in SH-SY5Y neuroblastoma cells and primary human neurons: Protection against neurocytotoxicity elicited by dopamine, 6-hydroxydopamine, 4-hydroxy-2-nonenal, or hydrogen peroxide

“…8). In addition, induction of NQO1 may also indirectly contribute to D3T-mediated cytoprotection against H 2 O 2 toxicity via maintaining cellular levels of ubiquinol and vitamin E. As stated above, ubiquinol and vitamin E are important cellular antioxidants in protecting against ROS-induced injury (Ross, 2004;Young et al, 2007).…”

Potent Upregulation of Glutathione and NAD(P)H:Quinone Oxidoreductase 1 by Alpha-lipoic Acid in Human Neuroblastoma SH-SY5Y Cells: Protection Against Neurotoxicant-elicited Cytotoxicity

“…In addition, induction of NQO1 may also indirectly contribute to LA-mediated cytoprotection against ROS/RNS toxicity via maintaining cellular levels of the reduced forms of vitamin E and ubiquinone, two important endogenous antioxidants [36]. In this context, both vitamin E and ubiquinone have been shown to be able to protect against ROS/RNS-induced injury [60][61][62].…”

Identification of ataxia‐associated mtDNA mutations (m.4052T>C and m.9035T>C) and evaluation of their pathogenicity in transmitochondrial cybrids

“…For many years now CoQ 10 , a highly mobile carrier of electrons and protons between the flavoproteins and the cytochrome system, has been investigated as a potential therapeutic agent to treat cardiovascular diseases, neurodegenerative diseases, and mitochondrial disorders. 24,36,48 It can modify respiratory chain function and reduce the level of cytotoxic metabolites, including ROS. However, although numerous beneficial outcomes, both experimental and clinical, have been reported in response to CoQ 10 supplementation, its full therapeutic potential is greatly limited by the lack of solubility in aqueous media.…”