Fig. 4

Effect of sAPPα expression on the development of amyloid pathology. a-c Congo red staining of coronal brain sections from (a) WT-control, (b) Tg-sAPPα and (c) Tg-control animals revealed an absence of amyloid plaques in WT-control brains, but extensive plaque formation in Tg-sAPPα and Tg-control brains. d-e No significant differences in plaque density were observed between Tg- sAPPα and Tg-control in the hippocampus (p = 0.316, d) or overlying neocortex (p = 0.297, E). f-i Human amyloid-β load in the hippocampus. f Soluble Aβ1–40 levels differed between groups (one-way ANOVA F(2,27) = 17.40, p < 0.001), with higher levels in in Tg-control animals compared to wildtypes (WT-control: 15.6 ± 1.6 ng/mg, n = 12; Tg-control: 50.7 ± 6.9 ng/mg, n = 6, post-hoc Tukey p = 0.001), but no effect of sAPPα treatment compared to Tg-control (Tg-sAPPα: 56.1 ± 7.1 ng/mg, n = 12, Tukey = 0.820). g Insoluble Aβ1–40 levels showed a significant overall group effect (F(2,28 = 10.70) and while there was no significant difference between WT-control and Tg-control (WT-control, 2.8 ± 0.3 ng/mg, n = 13, Tg-control, 5.5 ± 1.0 ng/mg, n = 6, Tukey p = 0.145), the levels were elevated in the Tg-sAPPα group compared to WT-control (Tg-sAPPα 7.9 ± 1.1 ng/mg, Tukey p < 0.001) and they were not different to Tg-control (Tukey p + 0.194). (H) Soluble Aβ1–42 levels did not show any differences between groups. i For the insoluble fraction, there was an overall group effect (F(2,28) = 20.47, p < 0.001, whereby Tg-controls showed the expected greater Aβ1–42 load (2.26 ± 0.46 ng/mg, n = 6) compared to WT-controls (0.31 ± 0.077 ng/mg, n = 13; Tukey p = 0.006) and this level was not significantly affected by sAPPα over-expression (3.25 ± 0.48 ng/mg, n = 12, Tukey p = 0.220). **p < 0.01, ***p < 0.001, Scale bar: 1 mm