Fig. 2

Analysis of the parenchymal Aβ plaque load. Differential effects of APOE genotype on Aβ plaque load and its reduction effected by 10D5 mAb treatment. Representative microphotographs of coronal brain sections through the somatosensory cortex (a) and the dorsal hippocampus (c) from untreated age-matched (Age control) mice, and mice receiving an isotype control IgG2a antibody TY11-15 or 10D5 anti-Aβ mAb. Aβ plaques were immunostained with an antibody against the N-terminus of Aβ following formic acid treatment of the sections. Unbiased analysis of the parenchymal Aβ plaque load in the brain cortex (b), and in the hippocampus (d) revealed by anti-Aβ immunostaining. Values shown in (b) and (d) represent mean ± SEM from 8 to 12 animals in TY11-15 and 10D5 mAb treated groups and 5 to 10 mice in Age control groups per APOE genotype. (b) and (d) p < 0.0001 (one-way analysis of variance); *p < 0.05, **p < 0.01, and ****p < 0.0001, TY11-15 control vs. 10D5 mAb treatment for matching APOE genotypes (Sidak’s post hoc test). Differences between Age control and TY11-15 groups were non-significant for all matching APOE genotypes (Sidak’s post hoc test); not shown on the graph. ^### p < 0.001 and ^#### p < 0.0001, TY11-15 APP/ε4 control vs. TY11-15 APP/ε2 or APP/ε3 controls (Sidak’s post hoc test). ^♦♦ p < 0.01, TY11-15 APP/ε2 control vs. TY11-15 APP/ε3 control (Sidak’s post hoc test). ⁺⁺ p < 0.01, 10D5 mAb treated APP/ε4 mice vs. 10D5 mAb treated APP/ε2 or APP/ε3 mice (Sidak’s post hoc test). Differences between 10D5 mAb treated APP/ε2 and APP/ε3 mice were non-significant (Sidak’s post hoc test); not shown on the graph. Scale bars 50 μm (A) and 75 μm (c)