In recent years much of the research conducted in the field of Parkinson's disease (PD) has been aimed at trying to elucidate the molecular mechanisms involved in the development of the rare familial forms of the disease, with the hope that an understanding of these mechanisms will shed some light into the pathogenesis of the more prevalent idiopathic form of the disease. These studies have implicated mitochondrial dysfunction in the pathogenesis of familial PD, either as a primary event, with disease causing mutations identified in genes encoding mitochondrial proteins, or as a secondary event. Thus, the role played by mitochondrial respiratory chain function in the pathogeneis of idiopathic PD, an area of research that was a main focus some 15-20 years ago, has come back to the forefront of the field. A number of studies have directly investigated respiratory chain function in a variety of tissues from idiopathic PD patients. Although abundant in number, these studies have provided contradictory results, which still require clarification. In this review we will examine the data indicating the presence of a respiratory chain defect in patients with idiopathic PD and attempt to link it with the pathways that have been implicated by familial studies.