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. 2011 Apr 20;31(16):6208–6220. doi: 10.1523/JNEUROSCI.0299-11.2011

Figure 1.

Figure 1.

CCR2 deficiency accelerates the onset of spatial and contextual memory deficits and aggravates cognitive impairment in APPSwe/PS1 mice. Spatial memory was assessed using the water T-maze test (a–d) in wild-type, CCR2−/−, APPSwe/PS1, and APPSwe/PS1/CCR2−/− mice aged from 3 to 12 months. The numbers of trials (a, b) and the latency (c, d) to accomplish the task were determined during the acquisition (a, c) and reversal learning phases (b, d). APPSwe/PS1/CCR2−/− mice exhibited an earlier and greater spatial memory decline than APPSwe/PS1 mice. The passive avoidance test was used to establish contextual memory deficit (e, f). The latency was determined at 3–12 months of age during the acquisition phase (e) and 24 h after the conditioning test (f) for each group. The latency to enter the dark compartment was already decreased at 6 months of age in APPSwe/PS1/CCR2−/− mice compared with the control groups of mice. Results are expressed as mean ± SEM; n = 8–16 per group; *p < 0.05, **p < 0.01, and ***p < 0.001. *Versus WT at same age; °versus CCR2−/− at same age; #versus APPSwe/PS1 at same age. (Two-way ANOVA was performed and, for each parameter analysis, revealed a significant interaction between the factors of age and genotype. Then, one-way ANOVA at each level of age was performed using Bonferroni's or Tamhane's post hoc test.)

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