Furthermore, recent studies have shown that several disease-associated amyloid aggregates such as α-synuclein (Parkinson’s Disease), Tau (Alzheimer’s disease and other tauopathies), amyloid-β (Alzheimer’s disease) and huntingtin (Huntington’s disease) are also capable of cross-cell transmission in a ‘prion-like’ manner (reviewed in [Aguzzi and Lakkaraju, 2016]). This evidence concerns the gene HTT and Alzheimer disease.