Coenzyme Q10 (CoQ) is an electron acceptor for complexes I and II in the mitochon-drial electron transport chain. It is necessary for energy production and particularly abundant in metabolically active cells such as in the brain. Complex I involvement in PD was first demonstrated in MPTP toxicity. Subsequent research showed that complex I activity is reduced in all PD subjects, even very early in the disease (47,48). Shults et al. (49) found reduced CoQ levels in mitochondria of PD subjects, which correlated with complex I activity. Prophylactic oral supplementation of CoQ partially inhibited MPTP-induced loss of striatal dopamine and dopaminergic axons of mice (50).
Shults et al. (51) conducted an 80-subject, multicenter, parallel design study comparing placebo, 300, 600, and 1200 mg of oral CoQ over 16 months. The total UPDRS scores improved with the 1200 mg dose compared with placebo. There was a trend (P = 0.09) between dosage and the mean UPDRS scores. These improvements were largely powered by part II (ADL section) of the UPDRS. There were no significant differences in the motor examination. The effect size was greatest at 16 months but changes in activities of daily living could be seen at one month. Adverse events were minimal. The assay of NADH to cytochrome-C reductase suggests increased endogenous complex I activity in subjects taking CoQ. A second small controlled trial also demonstrated a modest symptomatic benefit at four weeks (52).
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