DRESDEN, Germany -- Treating Parkinson's disease patients with the antioxidant coenzyme (CoQ10) boosts plasma levels of the substance but doesn't improve disease symptoms, reported investigators here.
DRESDEN, Germany, May 14 -- Treating Parkinson's disease patients with the antioxidant coenzyme (CoQ10) boosts plasma levels of the substance but doesn't improve disease symptoms, said investigators here.
In a placebo-controlled trial, patients who took CoQ10 supplements for three months had significantly greater plasma levels of the substance, touted for a purported ability to protect dopaminergic neurons, found Alexander Storch, M.D., of the Technical University of Dresden, and colleagues.
But at the end of the trial scores on the Unified Parkinson's Disease Rating Scale (UPDRS) were no better for patients who took the supplements than for those patients taking placebo, the researcher reported online in the July issue of Archives of Neurology.
"Since we did not find symptomatic effects of CoQ10 in Parkinson's disease, our study does not support the hypothesis that restoring the impaired energy metabolism of the diseased dopaminergic neurons leads to symptomatic benefits in Parkinson's disease," they wrote.
But their findings do not shut the door on CoQ10 for Parkinson's disease. It's possible that supplementation with the substance in doses higher than the 300 mg daily used in their study could be beneficial, they said.
Some researchers have speculated that a disorder of the mitochondrial respiratory chain might be involved in the development of Parkinson disease, on the basis, in part, of evidence that the analgesic opioid MPTP (1-methyl 4-phenyl 1,2,3,6-tetrahydropyridine), which causes parkinsonian syndrome, inhibits mitochondrial complex I activity.
In addition, investigators have detected reductions in mitochondrial complex I activity of 30% to 40% in the substantia nigra of the brains of people with Parkinson's, but not in other areas of the brain.
"CoQ10 has attracted attention concerning neuroprotective actions in neurodegenerative disorders linked to mitochondrial defects or oxidative stress, such as Huntington disease and Parkinson's disease," the authors wrote.
Oral CoQ10 had been shown to reduce the loss of dopamine and dopaminergic axons in the striatum of mice with MPTP-induced parkinsonian syndrome, they noted.
"On the other hand, CoQ10 might also improve dysfunctions of cells suffering from energy depletion and subsequently generate symptomatic effects as demonstrated in various mitochondrial disorders," they added.
To test their hypothesis, the authors conducted a randomized, double-blind, placebo controlled study involving patients in 13 German movement-disorder clinics.
They enrolled a total of 131 patients with Parkinson's who did not have motor fluctuations and were on a stable antiparkinsonian treatment regimen.
The patients, ranging in age from 40 to 75, were randomized to placebo or a nanoparticular formulation of CoQ10 delivered in 100-mg oral doses three times daily for three months, followed by a two month washout period. The patients were stratified at study outset according to levodopa treatment.
The primary outcome was the change in the sum score of the UPDRS part II and part III from baseline to three months. Secondary outcomes included scores on six instruments, including total UPDRS score, Hoehn and Yahr (Parkinson's staging) score, Schwab and England Activities of Daily Living score, Parkinson's Disease Questionnaire (PDQ39) score, Global Clinical Impression score, and Montgomery-Asberg Depression Rating Scale.
The analysis was by intent-to-treat with last observation carried forward for patients who were lost to follow-up.
A total of 55 patients in the placebo group and 51 in the CoQ10 group completed the protocol. The authors found that after the washout period them mean change in the sum of the UPDRS parts II and III scores were -3.69 among placebo-treated patients and -3.33 for the CoQ10-treated patients (P=0.82). In both groups, the change from baseline was significant, at P