Although Alzheimer’s disease arises predominantly as a sporadic condition of late adult life, there are rarer early-onset Mendelian forms caused by mutations in the APP gene or in genes (PSEN1 and PSEN2) known to alter its enzymatic cleavage. We now provide evidence that Alzheimer’s disease is also transmissible in certain circumstances and, therefore, that Alzheimer’s disease (like Aβ-CAA) has the full triad of etiologies (sporadic, inherited and rare acquired forms) characteristic of conventional prion diseases. This should further emphasize that the principles of prion biology have relevance for other neurodegenerative diseases involving the accumulation of diverse assemblies of misfolded host proteins, which may have propagating and neurotoxic forms. Our cases suggest that, similarly to what is observed in human prion diseases, iatrogenic forms of Alzheimer’s disease differ phenotypically from sporadic and inherited forms, with some individuals remaining asymptomatic despite exposure to Aβ seeds due to protective factors that, at present, are unknown.