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NEUROLOGY 1997;49:S26-S33
© 1997 American Academy of Neurology

Attempts to obtain neuroprotection in Parkinson's disease

C. Warren Olanow, MD, FRCP(C)

From the Department of Neurology, Mount Sinai School of Medicine, New York, NY.

Address correspondence and reprint requests to Dr. C. Warren Olanow, Department of Neurology, Mount Sinai School of Medicine, 1 Gustave Levy Place, Box 1137, New York, NY 10029.

Abstract.

It is suggested that oxidant stress is a contributing factor in the pathogenesis of Parkinson's disease (PD). Oxidant stress may contribute to cell death in PD because oxidative metabolism of dopamine has the potential to yield highly reactive and cytotoxic free radicals. Evidence for this hypothesis includes: (1) increased dopamine turnover with increased hydrogen peroxide formation; (2) decreased glutathione availability; and (3) increased reactive iron in the brains of patients with PD. Antioxidant therapies might be neuroprotective and could slow the clinical progression of the disease whereas metabolites of levodopa therapy may accelerate the rate of neuronal degeneration. Laboratory studies demonstrate that both selegiline and dopamine agonists can provide neuroprotective benefits. Selegiline-treated patients require less levodopa and have a delay in the progression of parkinsonian signs and symptoms. Dopamine agonists provide antiparkinson benefits and also diminish the need for levodopa.




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