In sum, while it has been shown that overexpression of α-synuclein transgenes leads to protein aggregation in normal cells, the study of native processes leading to aggregation in affected individuals has been hindered by the inaccessibility of human neurons in vivo, the limitations inherent in studying postmortem samples from PD patients, and the inability to accurately recapitulate human disease in transgenic models [47–49]. This evidence concerns the gene SNCA and Parkinson disease.