Parkinson’s disease is the most common neurodegenerative disorder after Alzheimer’s disease, preferentially affecting locomotor activities of elderly people. Although our knowledge concerning the pathogenesis of Parkinson’s disease is still limited, some environmental toxins have been postulated as candidate substances which accelerate dopaminergic neuronal death through impaired cellular metabolism, such as mitochondrial oxidative dysfunction or excessive effects of free radicals. However, there has been increasing evidence suggesting that genetic factors may play some part in the pathophysiological processes of this disease. For example, studies using PET indicated a significantly higher concordance rate for decreased striatal [¹⁸F] dopa uptake in monozygotic twins.1 Furthermore, recent complex clinical analyses, aimed at re-evaluating family histories of cases of Parkinson’s disease, showed a significantly higher incidence of parkinsonian symptoms among relatives. These findings suggest autosomal dominant inheritance of the disease.2 Under these circumstances, several genes have been proposed as candidate genes for Parkinson’s disease.3 However, the association of these candidate genes with the disease is still controversial.