Volume 73 Number 4 July 2006	back to contents

Address all correspondence to Joseph Jankovic, M.D., Professor of Neurology, Director, Parkinson's Disease Center and Movement Disorders Clinic, Baylor College of Medicine, Department of Neurology, The Smith Tower, Suite 1801, 6550 Fannin, Houston, TX 77030; email: josephj@bcm.tmc.edu

Presented at the First Annual Melvin D. Yahr Lecture to the Department of Medicine, Mount Sinai School of Medicine, New York, NY on December 13, 2004, and updated September 2005.

Abstract

Although levodopa remains the most effective symptomatic drug for Parkinson's disease (PD), its use is limited by the emergence of motor fluctuations and dyskinesias, particularly in young-onset patients. Dopamine agonists, catechol-O-methyltransferasee inhibitors and other anti-parkinsonian drugs have been found to diminish or prevent these complications and possibly to exert disease-modifying effects. The finding that the subthalamic nucleus (STN) and the globus pallidum internus (GPi) are abnormally active in PD has led to effective surgical treatments designed to improve patients' quality of life. The relative benefits of targeting STN or GPi with high-frequency stimulation are still being debated. Experimental therapeutics of PD include novel delivery systems, anti-apoptotic strategies and implantation of genetically engineered cells, and stem cells. Despite encouraging results from early pre-clinical and clinical studies, trials of human fetal grafts and intraventricular and intraparenchymal infusion of glial cell-line-derived neurotrophic factor have not shown clinically meaningful benefits. Future therapeutic strategies should focus not only on ameliorating the symptoms of PD, but also on neuroprotective or neurorescue therapies that can favorably modify the natural course of the disease and slow the progression of both motor and nonmotor manifestations of PD.

Key Words

Parkinson's disease, levodopa, dopamine agonists, dyskinesias.

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