Parkinson Disease: Protective treatments

From: www.parkinson.org

Current symptomatic treatments (PD medications) can significantly impact on the management of the disease. They do not, however, prevent disease progression. There is great interest in the development of neuroprotective therapies to halt the disease or delay its onset. Cell loss in the substantia nigra is the cause of symptoms of PD. The reason that it occurs is unclear. The occurrence of certain chemical reactions involving oxidation results in the production of substances (such as so-called free radicals or reactive oxygen species) that may be harmful to cells and lead to their deaths. Such oxidative stress may thus be important with regard to the development of PD. Neuroprotective treatments may be most helpful at an early stage of PD, and this stresses the need for finding a simple biological marker. This would enable treatment to be initiated at the preclinical or early clinical phase of the disease.

Selegiline is an inhibitor of the enzyme MAO-B (monoamine oxidase B). Since this enzyme breaks down dopamine, inhibiting it prolongs the action of dopamine in the brain, and may improve the symptoms of Parkinson's disease. It also has a mild antidepressant effect. While early studies of selegiline initially led physicians to believe that it may delay the progression of Parkinson's disease, currently there is no firm evidence that this is so. Nevertheless, there are theoretical grounds to believe it may slow the disease.

Levodopa: there is controversy as to whether this medication is toxic to neuronal cells or protective. There is no evidence that it worsens or slows the progression of Parkinson's disease.

Coenzyme Q-10: Cells need energy to survive and function. They contain mitochondria, which are “batteries” that produce energy. In Parkinson's disease, there seems to be a disturbance in the function of these batteries. Coenzyme Q10 seems to affect this energy-generating mechanisms in cells, although the exact mechanism remains a mystery. A recent study suggested that treatment with 1200 mg/day of coenzyme Q10 resulted in improvements in measures of motor function over the fixed period of the study when compared to lower doses of the same compound or to a placebo compound. Coenzyme Q-10 was also found to be safe in this trial. A larger trial sponsored by NIH and the Parkinson Study Group is underway which will test 1200mg or 2400mg versus a placebo compound.


Dopamine agonists have been shown experimentally to protect dopamine cells. They may have antioxidant effects, inhibiting free radical formation and scavenging free radicals. They may also slow programmed cell death (apoptosis) which may be accelerated in Parkinson's disease.

Experimental Treatments

Many patients inquire about "restorative" therapies, a category of procedures that includes transplantation of fetal cells or stem cells, growth factors, or gene therapy. The goal of these procedures is to correct the basic chemical defect of Parkinson's disease by increasing the production of dopamine in the brain. Although theoretically very attractive, much more laboratory work must be done in order to make cell transplantation or growth factor therapies practical and effective. At this time, the restorative therapies are experimental and are not available as treatment.