The causative link between α-synuclein and disease is supported by (a) the identification of mutations or multiplications in the α-synuclein gene (SNCA) in familial PD and polymorphisms in the SNCA locus as the commonest risk in sporadic PD [9]; (b) the propensity of monomeric α-synuclein to self-assemble into filaments, that resemble by electron microscopy those extracted from PD brain [4, 5] and (c) the evidence that increased expression or aggregation of α-synuclein in animals causes neuronal dysfunction or degeneration [10]. Here, SNCA is linked to Parkinson disease.