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. 2015 Jul 8;5:12059. doi: 10.1038/srep12059

Figure 1. Agtr1a deficiency decreases Aβ deposition in an Alzheimer’s disease transgenic mouse model.

Figure 1

(a) Comparison of amyloid deposition in the 14-month-old hAPP/Agtr1a+/+, hAPP/Agtr1a+/− and hAPP/Agtr1a−/− mouse brain by thioflavin-S staining. (b) Thioflavin-S-positive amyloid plaque number in the cortex and the hippocampus of 14-month-old mice. n = 4–8 hAPP/Agtr1a+/+ mice, n = 9 hAPP/Agtr1a+/− mice and n = 6 hAPP/Agtr1a−/− mice. (c) Quantification of Aβ42 plaque number in the cortex and hippocampus. n = 10 hAPP/Agtr1a+/+ mice, n = 9–10 hAPP/Agtr1a+/− mice and n = 8 hAPP/Agtr1a−/− mice. (d) Aβ42 and Aβ40 levels in the cortex of 14-month-old mice determined by ELISA. n = 5–9 hAPP/Agtr1a+/+ mice, n = 6–7 hAPP/Agtr1a+/− mice and n = 5–6 hAPP/Agtr1a−/− mice. (e) AT1a expression in hAPP/Agtr1a+/+, hAPP/Agtr1a+/− and hAPP/Agtr1a−/− cells was evaluated by immunoblot. (f) Expression of brain APP was evaluated by immunoblot analysis and densitometry. Mature and immature APP are indicated by arrows. (g) Thioflavin-S staining of brain sections from 20-month-old hAPP/Agtr1a+/+ and hAPP/Agtr1a+/− mice. (h) Quantification of thioflavin-S-positive amyloid plaques in the cortex and hippocampus of 20-month-old hAPP/Agtr1a+/+ and hAPP/Agtr1a+/− mice. n = 9 hAPP/Agtr1a+/+ mice, n = 9 hAPP/Agtr1a+/− mice. Error bars show means ± s.e.m., *P < 0.05, **P < 0.01, ***P < 0.001 by one-way ANOVA followed by post hoc Bonferroni test comparing with hAPP/Agtr1a+/+ mouse. Cropped immunoblots are presented and all samples were compared under the same experimental conditions.