Fig. 1

Analysis of the fibrillar plaque load. APOE genotype differentially modulates fibrillar plaque load and its reduction in response to 10D5 mAb treatment. a Representative microphotographs of Thioflavin-S (Th-S) stained coronal brain sections at the level of the rostral hippocampus from untreated age-matched (Age control) mice, and mice receiving an isotype control IgG2a antibody TY11-15 or 10D5 anti-Aβ mAb. Unbiased quantification of Th-S positive, fibrillar Aβ plaque load in the brain cortex (b) and in the hippocampus (c). Values shown in (b) and (c) represent mean ± SEM from 7 to 13 animals in TY11-15 and 10D5 mAb treated groups and 5 to 11 mice in Age control groups per APOE genotype. (b), and (c) 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 < 0.0001, TY11-15 APP/ε4 control vs. TY11-15 APP/ε2 or APP/ε3 controls (Sidak’s post hoc test). ^♦ p < 0.05, TY11-15 APP/ε2 control vs. TY11-15 APP/ε3 control (Sidak’s post hoc test). ⁺⁺⁺⁺ p < 0.0001, 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 750 μm (a)