While previous effort primarily employed transgenes expressing tau mutants linked to FTDP-17 (refs 9, 10, 11, 35, 36, 37, 42) that are sufficient to aggregate independent of the neuritic plaque, we developed a mouse model expressing human tau repeat domain that is capable of inducing the pathological conversion of mouse wild-type tau only in the presence of the neuritic plaque. The gene discussed is MAPT; the disease is semantic dementia.