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. Author manuscript; available in PMC: 2022 Jan 15.
Published in final edited form as: Mol Psychiatry. 2020 Jul 10;26(10):5766–5788. doi: 10.1038/s41380-020-0806-5

Fig. 6. CRISPR/SpCas9-HF1-mediated reduction of BACE2 copy number from three to two in the T21C5 hiPSC line provoked early AD-like pathology in organoids.

Fig. 6

a–c Early AD-like pathology was provoked in 41DIV T21C5Δ7 organoids, but was not detected in T21C5 parental organoids. a–b Treatment of the T21C5Δ7 with combined βI-IV (β-sectretase inhibitor) and compound E (γ-secretase inhibitor) from 20 to 41DIV completely prevented the formation of extracellular amyloid deposits. Staining with amyloid specific dye (AmyloGlo) and nuclear dye (DRAQ5). Scale bar 50 μm. c β- and γ-secretase inhibitor treatment highly significantly reduced the presence of TG3+ (pathologically conformed Tau) cells in T21C5Δ7 organoids compared with untreated T21C5Δ7 organoids. Scale bar: 20 μm. Error bars: SD, ****p < 0.0001. Only statistically significant differences are shown.