Fig. 5

Use of the Alzheimer’s disease (AD) cerebral organoid (CO) model for the evaluation of drug activity. COs were subjected to analysis by ELISA, western blotting, Amylo-Glo staining, and immunostaining at day 70. (a) Schematic diagram of the process of CO generation and drug treatment. (b) Effect of β-secretase inhibitor (BSI) and compound E (CE) treatment on the levels of Aβ1–40 and Aβ1–42 in the CAP COs. The data represents the mean ± standard error of the mean (SEM); ***P < 0.001 vs. DMSO; n = 8 per sample. (c) Detection of amyloid plaques in the CAP COs treated with or without BSI or CE using Amylo-Glo staining. Scale bar = 100 μm. (d) Effect of BSI and CE treatment on the levels of paired helical filament (PHF) tau and total tau in the CAP COs analyzed by western blot analysis in the lysates of each CO. The data represents the mean ± SEM; **P < 0.005 and ***P < 0.001 vs. DMSO; n = 3 per sample. (e) Representative immunohistochemistry images showing the PHF-tau and TUJ1 in the CAP COs treated with or without BSI or CE. Scale bar = 100 μm