In The News

 

Several prescription medications have shown promise in managing the symptoms of Parkinson's disease (PD). The drugs, though, frequently come with a host of side effects, and studies suggest better alternatives may be close at hand. It could be the answers lie in natural therapies, which may slow the disease's progression and possibly even decrease motor deficits associated with Parkinson's disease.

In an effort to assess a natural therapy in treating the illness, The National Institutes of Health (NIH) is funding a trial to study coenzyme Q10's ability to slow the progression of PD. Substantial evidence has indicated that mitochondria (energy-producing cell parts) are impaired in PD. Work in a Parkinson's disease-affected animal model indicated that dietary supplementation with coenzyme Q10, which is a natural part of all cells, might slow the progression of the disease. Those who are in its early stages, and thereby do not require levodopa (Sinemet) or other medication, are eligible to participate in the study.

Patients are given one of three doses of coenzyme Q10-300, 600 or 1200 mg per day-or placebo, meaning each subject has a three in four chance of receiving coenzyme Q10. Patients are examined for progress approximately every four months, with up to seven visits over 17 months. The study aims to determine whether evidence suggests that coenzyme Q10 can slow the progression of PD that afflicted patients typically experience.

Investigators at 10 medical centers, all of who are members of the Parkinson Study Group, are carrying out the study. The Parkinson Study Group is a consortium of over 50 of the leading clinical centers in PD in North America. The study is directed by the University of California, San Diego and the Clinical Trials Coordination Center at the University of Rochester.

On another front, researchers at Jefferson Medical College in Philadelphia have found that melatonin is a potential ally against the neuron damage found in the brains of people who have PD. Previous studies, which did not use live animals, showed that melatonin's strong anti-oxidant effects appear to prevent neuron death in tissue similar to that seen in people with Parkinson's. This is the first study using live animals to determine if protection applies outside a petri dish.

Injections of neurotoxic agents were given to rats, causing lesions to develop in their brains. Some rats developed large lesions and some developed moderate lesions, as the injections were regulated. All the rats displayed motor (movement) deficits that are typical in people with PD. The rats were given melatonin either 10 minutes prior to the injection or 30 minutes after it. Without exception, melatonin decreased motor problems. In rats with large lesions, the melatonin decreased motor deficits in 50%. All of the control rats continued to show motor problems. The highest success rate was evident in rats with only moderate lesions. All of the rats given melatonin 30 minutes after the injection displayed no motor deficits. The rats given melatonin 10 minutes prior to the injection were slightly less fortunate, with symptoms disappearing in 87% of them.

Typically recognized as a sleep aid, how is it that melatonin produces such an effect? Scientists believe it is due to melatonin's anti-oxidative effect that neutralizes oxidative effects, which are thought to cause neuron damage. Cells that are affected by oxidants are not believed to die right away, but they do go through a staged process. In theory, melatonin intercedes during one of these stages, thereby circumventing cell death.

Although promising, the doses used on the rats were extremely high. Researchers have hopes that, in the future, they can identify, isolate, and use the element in melatonin that carries these effects to develop a treatment for Parkinson's disease.