In order to further explore the effects of the mitochondria–AD hallmark interaction, Rhein and colleagues [54] conducted a quantitative proteomic analysis and functional assays in four different strains of mice: the single transgenic pR5 mice to model tau pathology, the double transgenic APP/PS2 that model the Aβ plaque pathology, and the triple transgenic mice (pR5/APP/PS2) that combine the Aβ and tau pathologies. The gene discussed is MAPT; the disease is Alzheimer disease.