Fig. 6

Use of Alzheimer’s disease (AD) neurons for the evaluation of drug activity. AD neurons were subjected to analysis by ELISA, western blotting, and immunostaining at day 50. (a) Schematic representation of the process of neuronal differentiation and drug treatment. (b) Effect of β-secretase inhibitor (BSI) and compound E (CE) on the levels of Aβ1–40 and Aβ1–42 in the lysates of CAP neurons. The data represents the mean ± standard error of the mean (SEM); ***P < 0.001 vs. DMSO; n = 4 per sample. (c) Effect of BSI and CE treatment on the levels of paired helical filament (PHF) tau and total tau in the CAP neurons analyzed by western blot analysis of the lysates in each neuron. The data represents the mean ± SEM; *P < 0.05 and ***P < 0.001 vs. DMSO; n = 3 per sample. (d) Representative immunostaining images of the PHF-tau and TUJ1 in the CAP neurons treated with or without BSI or CE. The bar graph represents the ratio of cleaved caspase-3 (cCASP3)-positive cells to the total number of cells as measured by DAPI staining. Mean ± SEM; **P < 0.005 vs. CmC (DMSO); ^#P < 0.05 and ^##P < 0.005 vs. CAP (DMSO); n = 3 per sample