Disease progression is assumed to be initiated by protein misfolding followed by amyloidal self-assembly of an extensive variety of pathological proteins and polypeptides3, such as β-amyloid and tau in Alzheimer’s disease (AD)4, 5, α-synuclein in Parkinson’s disease (PD)6, TAR DNA-binding protein (TDP-43) in amyotrophic lateral sclerosis (ALS)7 and the prion protein in Creutzfeldt-Jakob disease8. This evidence concerns the gene TARDBP and Parkinson disease.