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. 2021 Aug 28;142(5):807–825. doi: 10.1007/s00401-021-02361-9

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© The Author(s) 2021

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 3 — Impaired lipid profiles in apoE-deficient cerebral organoids. Lipidomics and cholesterol assay were performed on lysates from parental control and isogenic APOE^−/− iPSC-derived cerebral organoids at Day 30 and Day 90. a–b, Heatmaps of top 50 lipid species significantly altered by apoE-deficiency at Day 30 (a) and Day 90 (b) are shown. c, Overall composition of lipid species in the lysates of iPSC-derived cerebral organoids. d–j, Concentration of total lipid (d), fatty acyl chains in triacylglycerol (FA, e), triacylglycerol (TAG, f), phosphatidylethanolamine (PE, g), phosphatidylcholine (PC, h), free cholesterol (CHL-free, i) and cholesterol ester (CE) species (j) in the lysates were plotted. All lipid concentrations were normalized to the protein levels. Lysates and culture media from 3 cerebral organoids were analyzed as one sample. All data are expressed as mean ± SEM (n = 5 samples/each). Two-way ANOVA were performed to determine statistical significance. *p < 0.05, **p < 0.01, *** p < 0.001, **** p < 0.0001