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Fig. 3 | Molecular Neurodegeneration

Fig. 3

From: Alzheimer’s disease-like APP processing in wild-type mice identifies synaptic defects as initial steps of disease progression

Fig. 3

AAV-APP/PS1 mice show a production of human APP similar to AD patients, 3 months after injection. C57Bl/6 J mice (all males) were injected at 8 weeks of age either with AAV-CAG-PS1M146L (AAV-PS1 mice, n = 4), AAV-CAG-APPSL (AAV-APP mice, n = 4) or both vectors at the same doses as for the other two groups (AAV-APP/PS1 mice, n = 4). Non-injected WT mice (n = 4) and transgenic APP/PS1ΔE9 mice were also used and all animals were killed at 5 months of age. Human samples were obtained from late-onset AD cases (Braak 6, Thal 5) and age-matched controls. The hippocampus was the structure analyzed for all samples. a Representative western blot of human APP (6E10 antibody) between AAV injected mice (n = 3 per group), human samples (n = 5 per group) and transgenic APP/PS1ΔE9 mice (n = 3). b Densitometric analyses of the antibody immunoreactivity shown in panel (a). Bars represent means ± SEM and data were normalized with respect to GAPDH. Statistical analysis was performed by one-way ANOVA with Tukey’s post-hoc test: ***p < 0.001. Note that AAV-APP/PS1 mice and human AD cases have similar levels. c Representative western blot of total APP (APP C-ter antibody) between non-injected WT, AAV injected and APP/PS1ΔE9 mice. d Densitometric analyses of the antibody immunoreactivity shown in panel c. Bars represent means ± SEM and data were normalized with respect to GAPDH. Statistical analysis was performed by one-way ANOVA with Tukey’s post-hoc test: **p < 0.01

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