The pathogenesis of idiopathic Parkinson's disease (PD) is not known, but is thought to be multifactorial, deriving from environmental factors acting on genetically predisposed individuals with aging. Association studies of DNA polymorphisms are able to detect a genetic background predisposing to PD. Mechanisms as oxidative stress, xenobiotica toxicity and altered dopamine metabolism might lead to a selective cell death of most vulnerable nerve cells and represent the primary subject to be studied by DNA analysis. Furthermore, protein aggregation is likely to be a major cause for the disease. Recently it has been shown that α-synuclein is accumulated in Lewy bodies of sporadic PD and mutated in some rare families with an autosomal dominant trait of the disease (ADPD). The identification of further genes responsible for PD will subsequently lead to first insights into the pathogenesis of one of the most common neurodegenerative disorders in humans.