The majority of idiopathic PD cases are of the late-onset, sporadic form with cytoplasmic α-SYN aggregates, which suggests that increasing levels of aggregation and toxicity do not depend only on genetic mutations in SNCA. However, to date, studies attempting to elucidate the molecular mechanism of α-SYN aggregation have focused solely on the biochemical properties of mutant protein species found in rare familial forms of PD. This evidence concerns the gene SNCA and Parkinson disease.