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Fig. 2 | Translational Neurodegeneration

Fig. 2

From: Paroxetine ameliorates prodromal emotional dysfunction and late-onset memory deficit in Alzheimer’s disease mice

Fig. 2

Paroxetine treatment attenuated memory deficit and Aβ accumulation of APP/PS1 mice in the late period. a Schematic of fear condition test. b Freezing time in context A and context B of FCT for saline or paroxetine treated WT and APP/PS1 mice. n = 9–11. c Representative immunohistochemical staining shows Aβ immunoreactivity in the cortex of APP/PS1 mice that treated with saline or paroxetine. Scale bar, 100 μm. d Results of quantitative analysis of Aβ-positive neurons in the cortex of APP/PS1 mice that had been treated with saline or paroxetine. n = 10. Data are presented as mean ± SEM. *P < 0.05; ** P < 0.01; *** P < 0.001; two-way ANOVA with Sidak’s multiple comparison post hoc test (b) and unpaired t-test (d). e Representative western of tau phosphorylation in the cortex of 6-month WT and APP/PS1 mice are shown and quantified n = 9. Data are presented as mean ± SEM and determined by Student’s t test. f Results of GO Enrichment analysis on the set of differentially expressed genes (DEGs). The length of each bar indicates the log10 (P-value) and the vertical axis shows significantly enriched terms. g Venn diagram of three GO term (Left panel). Overlapped 5 genes with differential expression were shown by heatmap (Right panel)

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