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. 2022 Jul 5;145(12):4474–4488. doi: 10.1093/brain/awac236

Figure 2.

Figure 2

BBB dysfunction and BEC disruption presented at an early stage of Alzheimer’s disease pathogenesis in APP/PS1 mice. (A) Immunostaining of Aβ in the hippocampus of 2-, 4- and 9-month-old wild-type (WT) and APP/PS1 mice (scale bar = 500 µm). (B) Immunostaining of Fibrinogen and CD31 in the hippocampus of 2-, 4- and 9-month-old wild-type and APP/PS1 mice (scale bar = 20 µm). (C) Immunostaining of Cldn5 in the hippocampus of 4- and 9-month wild-type and APP/PS1 mice (scale bar = 20 µm). (D) Immunostaining of Glut1 in the hippocampus of 4- and 9-month-old wild-type and APP/PS1 mice (scale bar = 20 µm). Arrowheads indicate the markers of interest in APP/PS1 mice. (E–G) Quantification of Fibrinogen, Cldn5 and Glut1 in the hippocampus of 2-, 4- and 9-month-old wild-type and APP/PS1 mice. Data are presented as mean ± SEM, n = 5, *P < 0.05, **P < 0.01.