Fig. 5

CD36 deletion in BAM attenuates pial and parenchymal CAA in 15-month-old Tg2576 mice. Schematic drawing depicting the location of the pial and parenchymal vessels studied. A-B Pial CAA. A In vivo two-photon excited fluorescent images illustrating methoxy-XO4⁺ amyloid deposits (Cyan) around somatosensory cortex blood vessels (magenta) identified by retroorbital injection of 70 kDa Texas Red dextran. Methoxy-XO4⁺ Aβ deposits are reduced in CD36^−/− → Tg2576 compared to WT → Tg2576 mice. B Pial CAA burden and smooth muscle fragmentation index in tangential cortical sections double labelled with the smooth muscle cell marker α-actin and the Aβ antibody 4G8. Smooth muscle cells are fragmented (arrows) near dense amyloid deposits (CAA burden; arrowhead) in WT → Tg2576 chimeras compared with WT → WT. The barographs show quantification of CAA burden (expressed as the ratio between 4G8 and α-actin immunoreactivity) and fragmentation (see methods). The correlation plot on the right, in which the individual data points in the CAA and fragmentation barographs were correlated, shows a significant linear correlation between CAA burden and smooth muscle cell fragmentation. Reduced CAA burden in CD36^−/− → Tg2576 chimeras is associated with a comparable reduction in the fragmentation index. C-D Parenchymal CAA burden in tangential cortical sections double labelled with α-actin or the endothelial marker Glut1 and thioS. The barograph shows quantification of CAA burden (expressed as the number of α-actin⁺ or Glut1⁺ thioS⁺ vessels/mm²) in intraparenchymal arterioles. α-actin is reduced in WT → Tg2576 but not in CD36^−/− → Tg2576 chimeras, and the number of α-actin⁺ thioS⁺ vessels is reduced in CD36^−/− → Tg2576 chimeras (C). The number of Glut1⁺ vessels is comparable between groups, but the number of Glut1⁺thioS⁺ vessels is reduced in CD36^−/− → Tg2576 chimeras (D). N = 5/group; two-way ANOVA with Tukey’s test; scale bars in A-D, 50 µm. Data presented as mean ± SEM