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Free-Radical Toxicity and Antioxidant Medications in Parkinson's Disease

CD Ciccone, PhD, PT, is Professor, Department of Physical Therapy, School of Health Science and Human Performance, Ithaca College, Smiddy Hall, 953 Danby Rd, Ithaca, NY 14850 (USA) (ciccone@ithaca.edu).

This excerpt was created in the absence of an abstract.

Parkinson's disease is a movement disorder characterized by the progressive degeneration of neurons located in the substantia nigra.^1,2 These neurons synthesize and secrete dopamine, and the loss of dopaminergic influence on other structures in the basal ganglia leads to the classic parkinsonian symptoms of resting tremor, bradykinesia, rigidity, and postural instability.^1,3 Pharmacologic treatment of Parkinson's disease traditionally has centered on administering medications that restore dopaminergic influence in the basal ganglia. The cornerstone of treatment usually consists of levodopa (L-dopa), which is the immediate precursor to dopamine.^1,2 Levodopa crosses the blood-brain barrier, where it is then converted to dopamine, thus helping reestablish dopaminergic effects, The administration of L-dopa can often produce dramatic improvements in parkinsonian symptoms, especially during the early stages of the disease.¹

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