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Fig. 4 | Molecular Neurodegeneration

Fig. 4

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

Fig. 4

AAV-APP/PS1 mice show a production of amyloid derivatives 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 at 5 (n = 3), 14 (n = 8) and 16 (n = 8) months of age were also used. 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 Comparative analysis of TBS-Tx soluble human βCTF levels by ELISA. Statistical analysis was performed by one-way ANOVA with Tukey’s post-hoc test: ***p < 0.001. A logarithmic scale was used. Note that AAV-APP/PS1 mice and human AD cases have similar levels. b-c Quantification (6E10 based MSD immunoassay detecting human Aβ species) of TBS-Tx soluble human Aβ42 (b) and Aβ40 (c). Statistical analysis was performed by one-way ANOVA with Tukey’s post-hoc test: ***p < 0.001, **p < 0.01. Note that AAV-APP/PS1 injected mice show higher levels of Aβ42 compared to human controls and reduced levels compared to late stage human cases. d Representation of the Aβ42/40 ratio. Note that no significant difference was detectable between AAV-APP/PS1 mice and human AD cases

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