ABSTRACT
INTRODUCTION Dopamine agonists have been used to treat Parkinson’s disease (PD) since the late 1970s (1). These agents were initially introduced as adjunctive therapy to levodopa. In the last 30 years, dopamine agonists have demonstrated therapeutic benefi t in all stages of PD, both in combination with levodopa and as monotherapy. Clinical, neuroimaging, animal, and cellular data suggest not only a levodopa-sparing effect and a delay in the incidence of motor fl uctuations, but also a potential neuroprotective effect (2-5). A number of hypotheses have been proposed including a reduction of free radical formation by limiting levodopa exposure or an increase in the activity of radical-scavenging systems, perhaps by changing mitochondrial membrane potential. In addition, some investigators suggest that dopamine agonists may provide neurotrophic activity. However, there is currently no defi nitive evidence of disease modifi cation beyond the delay of levodopa-induced motor complications.
