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Published Erratum
. 2022 Jan;143(1):119-121.
doi: 10.1007/s00401-021-02380-6.

Correction to: Apolipoprotein E regulates lipid metabolism and α‑synuclein pathology in human iPSC‑derived cerebral organoids

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Published Erratum

Correction to: Apolipoprotein E regulates lipid metabolism and α‑synuclein pathology in human iPSC‑derived cerebral organoids

Jing Zhao et al. Acta Neuropathol. 2022 Jan.
No abstract available

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Figures

Fig. 4
Fig. 4
ApoE2 and apoE3, but not apoE4, partially rescue α-synuclein accumulation in apoE-deficient cerebral organoids. The APOE−/− iPSC-derived cerebral organoids at Day 90 were treated with conditioned media of immortalized astrocytes from APOE2-target replacement (TR), APOE3-TR, or APOE4-TR mice for 5 days. Conditioned media from Apoe-KO astrocytes were used as a control. a, A schematic workflow of the rescue experiments. b–i, Amounts of EEA1 (c), LAMP1 (d), GCase (e), LIMP1 (f), Plin2 (g), αSyn (h) and p-αSyn (i) in the RIPA fraction of the cerebral organoids after treatments were quantified by Western blotting. j–l, Amounts of total αSyn (k) and p-αSyn (l) in the SDS fraction of cerebral organoids after treatments were quantified by Western blotting. All data were normalized to β-actin levels. 3 cerebral organoids were pooled and analyzed as one sample. All data are expressed as mean ± SEM (n = 5 samples/each). Experiments were repeated in three independent differentiation batches. One-way ANOVA was performed to determine statistical significance. **p < 0.01, ****p < 0.0001, n.s., not significant

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