Almost 200 years after James Parkinson (1817) first reported the disease that bears his name, our understanding of the cognitive deficits caused by Parkinson’s disease (PD) is still incomplete. In some patients, cognitive problems are severe; approximately 10% to 15% PD patients meet the criteria for dementia (Mayeux et al., 1988; Growdon et al., 1990). Even in nondemented patients, however, specific cognitive deficits are striking. Approximately 60% of nondemented patients are impaired in at least one cognitive domain (Growdon et al., 1990), including cognitive control processes, memory, verbal ability, and visuospatial functions. Further, cognitive dysfunction may correlate with other clinical variables. For example, late-onset patients manifest cognitive deficits earlier than early-onset patients, even when additive contributions of disease duration and normal aging are taken into account (Locascio et al., 2003; Katzen et al., 1998). The administration of levodopa has also been shown to impair cognitive performance in PD (e.g., Cools et al., 2006), which may result from the selective over-dosing of neural regions that are relatively unaffected in PD.