Thus, as the case of prion disease, differences of lesions among α-synucleinopathies are thought to be caused by conformational heterology of α-synuclein assemblies, probably amyloid-like fibrils (Lau et al., 2020; Schweighauser et al., 2020; Shahnawaz et al., 2020). This evidence concerns the gene SNCA and synucleinopathy.