Furthermore, studies of PS19 mouse models in the background of human APOE KI or APOE−/− reported a more dramatic degree of neurodegeneration and brain atrophy, as well as a higher level of insoluble tau formation in 9 months old APOE4/PS19 mice when compared to APOE3/PS19 mice, and APOE knockout in this case completely abolished tauopathy-related neurodegeneration [110]. The gene discussed is APOE; the disease is tauopathy.