Fig. 7

GEE reduces tau and Aβ pathologies in 10-m-old AD offspring hippocampus. (a-c) GEE attenuates tau hyperphosphorylation at multiple AD-associated sites, as measured by western blotting and immunohistochemical staining (scale bar, 50 μm). (d,e) GEE decreases the Aβ1–40 level with reduced Aβ plaques in the cortex and hippocampus, as measured by ELISA and immunofluorescent staining (scale bars, 50 μm, from at least 4 independent experiments, unpaired t-test). (f,g) GEE activates AKT, as shown by increased phosphorylation at Thr308 (pT308AKT) with inhibition of GSK-3β determined by increased pS9GSK-3β and reduced pY216GSK-3β. The phosphorylation level of AKT and GSK-3β was normalized against total AKT and GSK-3β, respectively. Data are presented as the mean ± s.e.m. of at least 3 independent litters of mice, unpaired t-test (e and g), *P < 0.05, **P < 0.01 vs. Ctrl