Fig. 3: Differential transcriptional profiles and synapse pathology in the hippocampus of AD transgenic mice. | Molecular Psychiatry

Fig. 3: Differential transcriptional profiles and synapse pathology in the hippocampus of AD transgenic mice.

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

Fig. 3

A Venn and gene ontology diagrams illustrating the differentially expressed genes and enriched cellular pathways altered in the hippocampus of 6 month-old female APP (n = 8), Tau (n = 8) and APP/Tau mice (n = 10) compared with controls (WT, n = 11). B Biochemical analysis of pre- and post-synaptic proteins and tau (D1M9X antibody) in hippocampal lysates and purified synaptosomes of WT, APP, Tau and/or APP/Tau mice at 6 months (n = 8–11 mice/group). Data represent mean levels (fold change) normalized to β-tubulin ± SEM. Number of mice (male/female): 11 WT (6/5, white symbols), 8 APP (5/3, red symbols), 8 Tau (5/3, blue symbols) and 9 APP/Tau (5/4, grey symbols). C Confocal microscope images of cleared expanded hippocampal and BLA sections (expansion factor 3.63x) of 6 month-old WT and APP/Tau mice showing colocalization (yellow; quantification at the right graph) of postsynaptic Homer1 (green) and pTau (Ser 202; red) in the CA1 hippocampus but not in the BLA of APP/Tau mice. Right top insets are magnified images of the indicated squared regions. Scale bars: 10 μm and 36.30 μm (expanded). Statistics were determined by one-way ANOVA or Kruskal-Wallis tests followed by Dunnet’s or Dunn’s multiple comparisons tests according to the normality test, respectively (B) or by two-tailed Student’s t-test (C). *P < 0.05, **P < 0.01, ***P < 0.001 vs non-transgenic control group.

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