Co-enzyme Q10 hope for Huntington’s disease
Co-enzyme Q10 might be useful in preventing functional
decline in Huntington’s disease a new study shows. Researchers say that
although results are inconclusive, it is the first controlled trial to
find a trend towards a beneficial change in functional decline.
Dr Karl Kieburtz, University of Rochester medical
centre, New York, and colleagues, compared the efficacy of co-enzyme Q10,
remacemide (a drug in development), a combination of the two agents, or
placebo in 347 patients. Co-enzyme Q10 was given at a dose of 300mg twice
a day. Changes in patients’ total functional capacity were assessed at
baseline and every four or five months for 30 months.
Huntington’s disease is a neurodegenerative condition
characterised by involuntary movement (known as chorea), cognitive decline,
depression and irritability.
Neither co-enzyme Q10 or remacemide significantly
altered decline in patients’ total functional capacity.
However, patients treated with co-enzyme Q10 showed
a 13 per cent slowing in decline of total functional capacity. This difference
appeared after about one year of treatment, suggesting that it is an effect
on disease progression rather than an acute symptomatic effect, the researchers
comment.
However, they say that it is too early to recommend
co-enzyme Q10 for patients with the disease. “There were not enough patients
in the study to say that the slowing of decline was definitive. There
is a 15 per cent probability that it occurred by chance.” They add that
the benefit observed was small and that the financial costs of taking
such a high dose are considerable.
Co-enzyme Q10 had been shown to be of benefit in
another neurological disorder, familial ataxia, and is commonly sold as
an antioxidant nutritional supplement.
The results for remacemide, a glutamate receptor
blocker, were less positive. It had no effect on the rate of functional
decline. However, it did appear to reduce chorea, suggesting that glutamate
receptor blocking therapies might be useful in place of, or in addition
to, dopamine blocking or depleting agents, the researchers say.
They add that in addition to the possibility that
glutamate receptor toxicity does not play a major role in Huntington’s
disease, the failure of remacemide to impact on functional decline could
have been because of insufficient dosage or use at an inappropriate stage
of the disease (Neurology 2001; 57:397).
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