In humans, pathological deposition of insoluble amyloid aggregates has been shown to be associated with the development of Creutzfeldt-Jakob disease, Alzheimer’s disease, Parkinson’s disease, and T1D, where an increased islet amyloid polypeptide (IAPP) concentration may constitute a risk factor for β-cell destruction33,34. Here, IAPP is linked to Creutzfeldt Jacob disease.