Fig. 14

Left panel. Schematic diagrams of CuxO@EM-K synthesis and Peripheral Aβ clearance by CuxO@EM-K. (I) Preparation of erythrocyte membrane vesicles through a hypotonic treatment. (II) Incubation of erythrocyte membrane with Aβ-targeting molecule (DSPE-PEG-K) to prepare EM-K vesicles. (III) Fusion of EM-K vesicles onto CuxO (CuxO@EM-K). The resulting CuxO@EM-K captures Aβ in the blood followed by elimination of Aβ bound to CuxO@EM-K by the liver. Subsequently, clearance of peripheral Aβ facilitates a large efflux of Aβ from the brain into blood through the sink effect, leading to the reduction of brain Aβ burden; Right panel. Reduction of Aβ deposits and amelioration of memory deficits during treatment. A Representative images of Aβ staining in both the cortex and the hippocampus. Corresponding quantification of Aβ plaques in the cortex (B) and hippocampus (C). D Blood Aβ levels measured after treatment with CuxO@EM-K. E Escape latency to the platform in the training phase. F Time spent in the target quadrant. G platform entries. H Representative swimming paths of mice in the probe test. Data are mean ± SD (n = 6). ns: no statistical difference,*P < 0.05 and **P < 0.01. Reproduced with permission copyright 2020, American Chemical Society [149]