tcome of the study was to measure Parkinson impairment between the beginning of the study (week zero) and the end of the study (week 42). If levodopa accelerated disease progression, then those treated with levodopa would be expected to have more severe impairment than the placebo-treated group after the symptomatic benefit of levodopa had been eliminated through the 2-week washout phase. If levodopa slowed progression, then the levodopa-treated subjects would be expected to have less severe Parkinson disease than the placebo-treated group.

The clinical results showed a clear-cut benefit in favor of levodopa. Moreover, the higher the dosage, the more beneficial the result. A question remains, however, as to whether the 2-week washout of the drug was sufficient to account for the elimination of all of levodopa's symptomatic benefit.

The study also contained a brain imaging component that showed the opposite effect from the clinical research evaluations. Participants underwent evaluation of their dopamine neurons at the beginning of the study and again after 40 weeks of treatment. These results suggest that levodopa could possibly have accelerated the loss of dopamine neurons. These findings also raise the question as to whether levodopa treatment interfered with the imaging by temporarily altering the chemistry of the dopamine neurons.

The PSG (www.Parkinson-Study-Group.org) is a non-profit, cooperative group of Parkinson disease experts from medical centers in the United States and Canada who are dedicated to improving treatment for persons affected by Parkinson disease.

The National Institutes of Health and the Department of Defense's Neurotoxin Project provided financial support for this study, known as the ELLDOPA (Earlier versus Later LevoDOPA Therapy in Parkinson Disease) Study. Teva Pharmaceuticals Industries of Netanya, Israel, which markets generic levodopa, provided the s
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Contact: Karen Zipern
kz2110@columbia.edu
212-305-9746
Columbia University Medical Center
8-Dec-2004

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