SNCA and Parkinson disease: These patient samples display increased amount of shorter, alternatively spliced isoforms of SNCA: increased expression of SNCA isoforms lacking exon 4 leads to the formation of stable tetramers and neuroprotection, while increased expression of SNCA isoforms lacking exon 6 or both 4 and 6 leads to the formation of unstable heterotetramers that dissociate easily, thus resulting in the accumulation of toxic oligomers and increased PD risk [57].