Mitochondrial dysfunction as a result of α-synuclein accumulation has been implicated in PD pathogenesis and, thus, we have investigated the consequences of the overexpression of the Drosophila Bcl-2 homologue Buffy. The analysis of climbing over the lifespan of the flies has been applied to determine the role of the various gene products in rescuing the α-synuclein-induced phenotypes [12, 54–56]. The gene discussed is SNCA; the disease is Parkinson disease.