Fig. 1: Aβ potentiates early tau pathology in AD vulnerable brain regions in APP/Tau mice. | Molecular Psychiatry

Fig. 1: Aβ potentiates early tau pathology in AD vulnerable brain regions in APP/Tau mice.

From: Synaptic vulnerability to amyloid-β and tau pathologies differentially disrupts emotional and memory neural circuits

Fig. 1

Coronal brain sections of control (WT), APP, Tau and APP/Tau mice at 6 months (A) and 9 months (B) were stained with anti-human Aβ/APP (6E10; top) and pTau (Ser202, AT-8 (A) or CP13 (B); bottom) antibodies. Left images: Representative low and high (insets) magnified images of Aβ- and pTau-stained neurons in CA1 and CA3 hippocampus, entorhinal cortex (EC) and basolateral amygdala (BLA). Amyloid plaques in a 9 month-old APP/Tau mouse are visualized in the top right inset of CA3 region. Objective: 20×. Scale bar: 50 μm. Right diagrams: Quantification of Aβ-positive cells in WT (white symbols), APP (red symbols), Tau (blue symbols), and APP/Tau (grey symbols) mice. Data represent mean number ± SEM of APP/Aβ-and pTau-positive cells/μm2 (×10−5) (n = 3–4 slices/mouse). Number of mice (male/female), 6 months: WT (2/6), APP (1/5), Tau (0/5) and APP/Tau (3/5); 9 months: WT (6/6), APP (5/6), Tau (5/5) and APP/Tau (4-5/6-7). Statistical analysis was performed using one-way ANOVA or non-parametric Kruskal-Wallis tests according to the D’Agostino-Pearson omnibus normality test, followed by Tukey’s or Dunn’s post hoc test, respectively (A), and two-way ANOVA followed by Sidak’s (sex comparison) and Tukey’s (genotypes comparison within each sex) multiple comparison tests (B). *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001 vs WT or the indicated group.

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