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Fig. 7 | Molecular Neurodegeneration

Fig. 7

From: APOE Genotype Differentially Modulates Effects of Anti-Aβ, Passive Immunization in APP Transgenic Mice

Fig. 7

Quantitative analysis of perivascular hemosiderin deposits. APOE genotype differentially modulates occurrence of hemosiderin deposits and their increase during Aβ immunotherapy with APOE ε2 and APOE ε3 alleles having adverse and protective effects, respectively. Shown are means (± SEM) for counts of all brain perivascular hemosiderin deposits (a), small perivascular hemosiderin deposits (<15 μm in diameter) (b), large perivascular hemosiderin deposits (≥15 μm in diameter) (c), and perivascular hemosiderin deposits in the thalamus presented as per cent of all brain deposits (d) (n = 5-11/group). Hemosiderin deposits were counted on every tenth brain coronal cross-section along the entire rostro-caudal axis of the brain. (a) through (d) p < 0.0001 (one-way analysis of variance); *p < 0.05, **p < 0.01, ***p < 0.001, and ****p < 0.0001, TY11-15 control vs. 10D5 mAb treatment for matching APOE genotypes (Sidak’s post hoc test). + p < 0.05, and ++++ p < 0.0001, 10D5 mAb treated APP/ε2 mice vs. other 10D5 mAb treated APP/ε3 or APP/ε4 mice (Sidak’s post hoc test). ♦♦ p < 0.01, and ♦♦♦♦ p < 0.0001, 10D5 mAb treated APP/ε3 mice vs. 10D5 treated APP/ε4 mice (Sidak’s post hoc test). p < 0.05 APP/ε2 TY11-15 control vs. APP/ε3 TY11-15 control (Sidak’s post hoc test). Differences between Age control and TY11-15 groups were non-significant for all types of hemosiderin deposits for matching APOE backgrounds, so were differences in the count of large hemosiderin deposits between TY11-15 control and 10D5 mAb treated APP/ε3 and APP/ε4 mice (Sidak’s post hoc test); not shown on the graph

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