Fig. 4

A40-POs treatment restored the BBB phenotype. PCC for the colocalization of LRP1 and endothelial cells (CD31) (a). Analyzis was performed on images derived from three independent experiments, with 6–7 vessels studied per trial (statistical analysis performed via unpaired t-tests, **** p < 0.0001). Aβ content in cerebrovasculature (b) and parenchyma (c) quantified by ELISA. ELISA measurements of vascular and parenchymal LRP1, PACSIN2, and Rab5 levels in wild-type, Sham APP/PS1, and APP/PS1 mice after A40-PO treatment (d). STED microscopy imaging of LRP1 (white), Aβ (red), and vessel wall (green). After treatment, Aβ deposits around the BBB are cleared, and notable Aβ signals are present within the vascular lumen (e). For b, c, and d, statistical significance was determined via one-way ANOVA, *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001, n ≥ 3