Fig. 2

The constitutive deletion of APMAP worsens spatial memory and increases the hippocampal Aβ plaque load in AD mice. a, b In the Morris water maze, 20-month-old Alzheimer’s disease (AD) mice depleted for APMAP (ko/ko AD; n=5; 2 females and 3 males) exhibited poorer escape learning during training trials (repeated measures ANOVA: distance to platform, F_3,21=8.426 *p<0.05 Day 1 versus Day 4; treatment effect F_1,21=7.290, #p<0.05 +/+ AD versus ko/ko AD at day 4) (a), and spent significantly less time in the target quadrant during probe test (b) compared to AD control mice (+/+ AD; n=4; 1 female and 3 males). c Heat maps describing the spatial distribution of the two groups of animals during the probe trial. Arrows indicate release points; the solid circle indicates the platform position. d Aβ1-40 peptides were estimated by ELISA in whole brain SDS extracts prepared from the right hemispheres of 9-month-old APMAP-KO/AD mice (ko/ko AD; n=7 females) and age-matched wild-type control littermates (+/+ AD; n=4 females). e The detection of Aβ plaques was performed by immunohistochemistry (IHC) in the hippocampi of the left hemispheres of the same mice as in (d). f Representative microscopic images of coronal sections of hippocampi stained by IHC for the detection of Aβ deposits (in black). Student’s t-test was applied for statistical analyses in panels d and e, with * p<0.05