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. Author manuscript; available in PMC: 2014 Mar 1.
Published in final edited form as: Nat Neurosci. 2013 Aug 11;16(9):1299–1305. doi: 10.1038/nn.3486

Figure 7. Spatial memory deficits in APP/PS1 AD model mice are alleviated by deleting eIF2α kinase GCN2.

Figure 7

(a) Escape latency in the Morris water maze plotted against the training days. APP/PS1 mice (black circles, n=8) were slower to learn than WT mice (open squares, n=9), APP/PS1/GCN2 KO (grey squares, n=9) or GCN2 KO mice (grey triangles, n=12). Repeated measures ANOVA followed by a post hoc Bonferroni multiple comparison test, p= 0.0014, F(3, 37)=9.960. APP/PS1 vs WT: p<0.01, t=4.532; APP/PS1 vs APP/PS1/GCN2 KO: p<0.05, t=3.360; APP/PS1/GCN2 KO vs WT: p>0.05, t=1.172. (b) Percentage of time spent in the target quadrant during a 60 second probe trial of MWM test. One-way ANOVA, p = 0.0261, F=3.584. (c) Frequency of platform crossing during a 60 second probe trial of MWM test. One-way ANOVA, p = 0.0144, F=4.057. Number of platform crossing of APP/PS1/GCN2 KO mice is not significantly different from that of WT mice; APP/PS1 vs APP/PS1/GCN2 KO: p=0.0526. **p< 0.01. (d) In the visible platform test no difference was observed for escape latency among the four genotypes of mice. Repeated measures ANOVA, p=0.3735. F=1.500.