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. 2020 Jun 5;11:1029. doi: 10.3389/fimmu.2020.01029

Figure 1.

Figure 1

Characterization of cerebral plaque load and Aβ species in the APP-PS1 transgenic mouse model. (A) Representative images of Thioflavin-S staining of coronal sections from APP-PS1 transgenic (tg) mice at different ages. First occasional plaques are observed at 6 months of age in cortex and anterior hippocampus (white arrows). Diffuse staining in corpus callosum and other white matter bundles is non-specific, as it is observed in non-tg mice as well. Scale bar = 0.8 mm. Yellow box (0.33 mm2) shows area used for quantification. (B) Quantitative analysis of plaque load in the cortex shows progressively increased beta-amyloid plaque numbers with age. Only significant differences between pre-plaque stage (3 m) and other plaque pathology stages are shown. (C) Schematic of identified stages of beta-amyloid pathology progression in APP-PS1 tg mice. (D) MSD-analysis of sequential protein extracts from prefrontal cortex reveals that TBS and SDS-soluble Aβ1-42 species start to accumulate already at 8 months of age. Each symbol represents data from one tg mouse. Only significant differences between pre-plaque stage (3 m) and other plaque pathology stages are shown. 3 m, n = 8; 6 m, n = 8; 8 m, n = 8; 14 m, n = 8; 20 m, n = 8. (Data are shown as mean ± SD, *p < 0.05, ***p < 0.001, ****p < 0.0001, one-way ANOVA with Bonferroni's multiple comparisons test).