Treatment of rats with rotenone has been proposed in the year 2000 to provide an animal model of idiopathic Parkinson's disease. We review here the experience that has been gained meanwhile with this model. The published data suggest that the model does not ideally reproduce the pathophysiology of Parkinson's disease, that Rotenone treatment does not cause a purely neurodegenerative concondition, that the Rotenone model does not ideally recapitulate the motor symptoms of Parkinson's disease, that degeneration of the dopaminergic neurons is highly variable, that striatal neurons appear to degenerate more consistently than neurons in the substantia nigra, and that cytoplasmic accumulation of the tau protein is more abundant than alpha-synuclein aggregation in severely lesioned animals. In summary, these data suggest that Rotenone-treated rats model atypical Parkinsonism rather than idiopathic Parkinson's disease.