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Fig. 5 | Molecular Neurodegeneration

Fig. 5

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

Fig. 5

Characterization of CCA. The APOE ε2 allele is associated with increased CCA incidence. a Demonstration of CCA in the thalamus of APP/ε2 mice receiving TY11-15 isotype control IgG2a antibody or 10D5 anti-Aβ mAb. Arrowheads indicate numerous Aβ immunopositive capillary vessels (<8 μm in diameter). An arrow in the left panel points at the vessel, which wall is also Aβ immunopositive, but which was not counted as a capillary as its diameter exceeded the assumed capillary size cutoff. There is noticeable reduction in the density of Aβ immunoreactive capillaries following 10D5 mAb treatment shown on the right panel. Quantitative analysis of CCA. Shown are means (± SEM) for counts of Aβ immunopositive capillaries per mm2 in the brain cortex (b) and the thalamus (c) from 5–8 brains per APOE genotype and 3 sections per brain. p < 0.0001 (one-way analysis of variance) in (b) and p < 0.0001 (Kruskal-Wallis H test) in (c); *p < 0.05, and ****p < 0.0001, TY11-15 control vs. 10D5 mAb treatment for matching APOE genotypes (Sidak’s post hoc test in [b] and Dunn’s multiple comparison post hoc test in [c]). + p < 0.05, +++ p < 0.001 and ++++ p < 0.0001, TY11-15 APP/ε2 control vs. TY11-15 APP/ε3 or TY11-15 APP/ε4 control groups (Sidak’s post hoc test in [b] and Dunn’s multiple comparison post hoc test in [c]). # p < 0.05 in (b), TY11-15 APP/ε3 control vs. TY11-15 APP/ε4 control (Sidak’s post hoc test). Differences between Age control and TY11-15 control for matching APOE genotypes in (b) and (c) were non-significant; not shown on the graph. Scale bar 20 μm (a)

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