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Fig. 1 | Cell & Bioscience

Fig. 1

From: β-amyloid protein induces mitophagy-dependent ferroptosis through the CD36/PINK/PARKIN pathway leading to blood–brain barrier destruction in Alzheimer’s disease

Fig. 1

The APP/PS1 mouse BBB is damaged, pericytes are reduced, and CD36 expression is reduced. Pericytes express CD36 and colocalize with Aβ1. A PET/CT scan images of mice in each group. Brain glucose metabolic images of the APP/PS1 mice and the WT mice (taken 0–1 min after 18F-FDG injection). B The mean standardized uptake value (SUV) (n = 3). C Protein expression levels of PDGFRβ, NG2, CD36, and LRP1 in brain tissue. DG Semiquantitative analysis of PDGFRβ, NG2, CD36, and LRP1 protein levels. The data are presented as the means ± SD. H Immunohistochemical (IHC) staining shows the formation of amyloid plaques composed of Aβ. I Immunofluorescence showed that there were fewer APP/PS1 mouse endothelial cell (GLUT1 pink label)-covered pericytes (PDGFRβ green label) than those of the WT mice. J Fluorescence semiquantitative analysis of pericytes and endothelial cells. We randomly selected six 200 µm visual fields for statistical analysis (6 areas of the cortex and hippocampus were used for image acquisition). K Immunofluorescence shows that CD36 (pink) and Aβ (green) are colocalized in pericytes (red). Blue indicates DAPI. (##p < 0.01, ###p < 0.001 compared with the WT group, ΔΔp < 0.01 compared with the APP/PS1 6 mo group, n = 6)

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