Fig. 3. Aged ANKS1A KO brains exhibit increased immune cells. (A) A representative image of the CCM-like vessel lesions shows CD68-positve macrophages in the neocortex of aged ANKS1A-deficient mice (scale bar, 10 μm). The data were quantified and presented as means±SD (N=3 per group, n=8 sections). (B) A representative image of the CCM-like vessel lesions shows CD45-positive leukocytes in the neocortex of aged ANKS1A-deficient mice (scale bar, 10 μm). The yellow dotted box is enlarged in the right panels to show that the CD45-positve leukocytes contain DAPI staining (scale bar, 2 μm). The data were quantified and presented as means±SD (N=3 per group, n=8 sections). (C) The white arrow indicates a dilated focal cavity due to the CCM-like lesion (scale bar, 10 μm). The intensity of Aquaphorin 4 were quantified and presented as means±SD (N=3 per group, n=8 sections). (D) The size of CCM-like vessel lesions in aged ANKS1A-deficient mice were quantified (N=3 per group, n=21 sections). (E) The ZO-1 positive endothelial tight junctions are reduced in the dilated focal cavity of aged ANKS1A-deficient brains (scale bar, 2 μm). The arrow indicates a dilated focal cavity due to the CCM-like lesion. The data were quantified and presented as means±SD (N=3 per group, ANKS1A+/+ n=7, ANKS1A-/- KO n=5 sections).
© Exp Neurobiol
