Compelling evidence suggests that a defect in energy metabolism may play a role in the pathogenesis of various degenerative disorders including Parkinson's disease and Huntington's disease. The behavioural and neuropathological consequences in primates of chronic systemic administration of mitochondrial toxins which impair oxidative metabolism are of considerable interest. In the past few years observations have been published describing the behavioural, biochemical and histological consequences of chronic low-dose systemic administration of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine or 3-nitropropionic acid in baboons. The results of these studies strongly support the view that chronic energy metabolism impairment is involved in the pathogenesis of Parkinson's and Huntington's diseases.