Despite this, recentwork has demonstrated that these variants display distinct aggregationpropensities−,  and MSA-associated single nucleotide polymorphismsin the noncoding regions of the SNCA gene lead toupregulation of αSynΔ5. Alongwith evidence that this variant is indeed translated in the brain, this highlights the importance of better understandingof the amyloid formation mechanisms of these variants and their rolesin the pathogenesis of synucleinopathies. This evidence concerns the gene SNCA and synucleinopathy.