Alzheimer’s disease is the result of a complex interplay between amyloid-beta and tau proteins: the neuronal loss caused by tau coupled with the neuronal hyperexcitability caused by amyloid beta could have the effect of spreading tau outside zones of amyloid deposition, leading to differential tissue distributions of the two proteins, in line with recent cellular and neuroimaging data [29, 30]. The gene discussed is MAPT; the disease is early-onset autosomal dominant Alzheimer disease.