ABSTRACT
Dopamine agonists (DA) have been used to treat symptoms of Parkinson’s disease (PD) since the late 1970s (1). These agents were initially introduced to supplement the beneficial effect and possibly reduce the incidence of longterm complications of levodopa. In the last 30 years, methodical investigations of DA have demonstrated therapeutic benefit in all stages of PD both in combination with levodopa and as monotherapy. More recently, positron emission tomography (PET) and single photon emission computed tomography (SPECT) imaging have demonstrated possible benefit in patients randomized to a DA when compared to subjects receiving levodopa (2-4). Increasingly, clinical, animal model, and cellular data suggest not only a levodopa-sparing effect and a delay in the incidence of motor fluctuations, but also a potential neuroprotective effect (5). A number of hypotheses regarding this phenomenon have been proposed. These include reduction of free radical formation by limiting levodopa exposure or increase in the activity of radical-scavenging systems, perhaps by changing mitochondrial membrane potential. In addition, some investigators suggest that DA may enhance neurotrophic activity. However,
there is currently no evidence of neurological improvement clinically, using trial designs with sufficient duration and washout periods to assess neurological status beyond therapeutic response.
