Fig. 1

Amyloid pathology aggravates tau-seeded tau pathology and propagation. a Schematic overview of the tau-seed model. Tau-seeding is performed at 4 months of age in F⁻/T⁺ (PS19) or F⁺/T⁺ (5xFAD/PS19) mice. Pathological analysis occurs at 7 months of age. b Representative images of the ipsi- and contralateral frontal cortex (scale bar = 250 µm) and hippocampus (scale bar = 500 µm) of F⁻/T⁺ and F⁺/T⁺ mice following tau-seeding, and their non-seeded controls at 7 months (3 months post-injection), immunohistochemically stained with anti-phospho-tau (pSer202/Thr205) antibody AT8. c Quantitative analysis of AT8 signal in the ipsi- and contralateral cortex and hippocampus of tau-seeded F⁻/T⁺ (n = 8) and F⁺/T⁺ mice (n = 6) compared to non-seeded F⁻/T⁺ and F⁺/T⁺ mice (n = 9, n = 9). Two-way ANOVA, Tukey’s test for multiple comparison. Data are presented as mean ± SEM; **p < 0.01; ***p < 0.001; ****p < 0.0001 d Gallyas Silver and Thioflavin S (ThioS) staining concurred with AT8 staining, indicating formation of mature NFTs. ThioS, binding β-sheet structures, and silver staining, both stain Aβ pathology and tau pathology concomitantly, preventing quantitative analysis of tau pathology only. These stains are presented to demonstrate the presence of aggregated tau. Scale bar = 100 µm. (FrCx = frontal cortex; CA1 = cornu ammonis 1; Sub = subiculum)