Do cognitive changes of Parkinson's disease result from dopamine depletion?

Cognitive changes have long been observed in patients with Parkinson's disease: visuo-spatial deficits, memory disorders, dysexecutive syndrome. Given the modulatory role of the basal ganglia and related structures, these deficits might result from more fundamental disorders concerning the allocation of attentional resources, the temporal organization of behavior, the maintenance of representations in working memory or the self-elaboration of internal strategy, all of which resemble dysfunctions of processes that are commonly considered to be controlled by the frontal lobes. This suggests a functional continuity between the basal ganglia and association areas of the prefrontal cortex. The recent description in primates of parallel, segregated loops that interconnect well defined subregions of the basal ganglia to discrete areas of the prefrontal cortex via the thalamus may give some support to this hypothesis.