It is therefore likely that in α-synucleinopathy diseases where mutations in SNCA gene are not a contributing factor, αS does not represent a typical  prion, where the protein alone is capable of propagating the disease as is the case with the prion protein in diseases like kuru and Creutzfeldt-Jakob disease, but requires a permissive environment or additional disruption of cellular health. This evidence concerns the gene SNCA and Creutzfeldt Jacob disease.