The protein α-synuclein was first isolated from human brain tissue during the early 1990s.1 Its role in PD only became apparent in 1997, when a mutation in the α-synuclein gene was discovered in groups of patients with a rare, autosomal dominant form of familial parkinsonism,2 and the major component of Lewy bodies was identified as α-synuclein.3 While the precise functional mechanisms of α-synuclein are still being elucidated, it appears to interact with and affect various proteins involved with vesicle formation, vesicle pools, and pore opening of the presynaptic terminal.1,4,5
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