In addition to confirming that genetic deletion of CatD triggers profound intracellular accumulation of human Aβ in mice overexpressing human amyloid precursor protein (hAPP), we report that CatD-KO mice exhibit a variety of histological and biochemical features consistent with robust tauopathy, including Gallyas silver staining strongly resembling mature NFTs in AD brain, widespread phospho-tau immunoreactivity, and prominent increases in sarkosyl-insoluble, hyperphosphorylated tau exceeding the levels present in an aggressive transgenic mouse model of tauopathy—all by ∼ 3 weeks of age. This evidence concerns the gene MAPT and tauopathy.