α-synuclein fibrillar polymorphs, Tau and Aß 1–42 fibrillar assemblies have been shown to propagate, amplify and trigger the formation of protein deposits reminiscent of those present within the central nervous system of patients developing synucleinopathies, tauopathies and amyloid plaques after injection intracerebrally, intramuscularly, intraperitoneally or within the blood stream of model animals. This evidence concerns the gene SNCA and tauopathy.