PET Investigations of Parkinson’s Disease

Abstract

Degeneration of nigrostriatal neurons with subsequent striatal dopamine deficiency leads to Parkinson’s disease (PD) with tremor, slowness, reduced spontaneous movement, stiffness, and postural instability (Hoehn, Yahr, 1967). The progression of PD is gradual but relentless; fortunately, symptomatic treatment provides substantial relief, especially early in the course of the disease. As yet, the pathogenesis of the substantia nigral degeneration remains unknown although a specific defect in the α-synuclein gene on chromosome 4 has been found in a few rare extended families with familial parkinsonism (Polymeropoulos et al., 1997). However, gene-sequencing analysis has not identified a defect in this gene in many other families with PD (Chan et al., 1998; Parsian et al., 1998), and the link between a genetic defect and the pathophysiology of the disease remains an area of intensive research. Furthermore, the functional consequences of the nigrostriatal degeneration on the development of the clinical manifestations of the disease and the response to pharmacotherapy are other areas of active investigation.