Pathologically, Alzheimer and prion disease share hallmarks of disease progression: short toxic protein oligomers that form into extracellular plaques containing both PrPSc and Aβ, early loss of dendritic spines and synaptic plasticity associated with learning deficits, tau hyperphosphorylation and neurofibrillary tangles, dysfunction in metal homeostasis, gliosis, neuronal apoptosis and dementia [41]–[44]. The gene discussed is MAPT; the disease is dementia.