Figure 1. Autologous EGCs induced Aβ plaques degradation.

(a) Diagram showing Aβ_(1–42) peptide infusion, EGCs isolation from the appendix, their transplantation in rat brain, and the time schedule for in vitro and in vivo measurements. (b) The injection of Aβ_(1–42) peptide causes a time-dependent amyloid deposition in frontal cortex and hippocampus of treated rats; in EGCs transplanted rats a time-dependent reduction of Aβ plaques was instead observed (n = 10 per group; congo red staining, scale bar: 500 μm). (c) The graphs show that Aβ burden time-dependently increased in sham versus vehicle-treated rats and that EGC transplantation resulted in a significant inhibition of Aβ accumulation. In the frontal cortex (left panel) and the hippocampus (right panel) Aβ burden was significantly higher in sham (black bars) than in vehicle-treated rats (white bars) at 4 and 8 weeks (***P < 0.001), while in EGC-transplanted rats it was significantly reduced (°P < 0.05 and °°°P < 0.001 vs. sham group). (d) Representative scans of ¹¹C-labeled Pittsburgh Compound-B positron emission tomography; Standardized uptake values (SUV) images of Aβ binding within the region of interest (ROIs) in the frontal cortex (COR) and hippocampus (HIP) of rats (n = 6 per group). (e) Relative SUVs for selected ROIs in the cortex (left panel) and hippocampus (right panel). Data were expressed as mean ± SEM; **P < 0.01, ***P < 0.001 vs. vehicle; °P < 0.05; °°° P < 0.001 vs. sham; two-way ANOVA.