In the last decade, evidence for such a prion-like behavior has been shown for several of the most prominent disease proteins, including α-Synuclein/SNCA (α-Syn; associated with Parkinson’s disease (PD) and other synucleinopathies), Tau/MAPT (associated with Alzheimer’s disease (AD), traumatic brain injury (TBI) induced tau pathology, and other tauopathies), the Aβ-peptide (associated with AD), huntingtin with extended polyglutamine stretches (HTT-polyQ; associated with Huntington’s disease (HD)), and TDP-43 (associated with amyotrophic lateral sclerosis (ALS)) [9,10]. This evidence concerns the gene MAPT and juvenile Huntington disease.