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. 2019 Mar 12;10(3):244. doi: 10.1038/s41419-019-1422-7

Correction: Aberrant iPSC-derived human astrocytes in Alzheimer’s disease

V C Jones 1, R Atkinson-Dell 2, A Verkhratsky 2,3, L Mohamet 2,
PMCID: PMC6414541  PMID: 30862780

Correction to: Cell Death & Disease 8:e2696

10.1038/cddis.2017.89

published online 23 March 2017

The original version of this Article contained an error in Fig. 1, in which a number of incorrect fluorescence images were inadvertently incorporated into the panel. The conclusions of the paper are not changed in any way by this correction, and the authors apologize for the inconvenience.

Fig. 1. Directed differentiation of healthy and AD-neural progenitor cells into cortical neurones.

Fig. 1

ac NPCs were seeded at 1 × 105 per well and propagated in monolayer culture for 6/7 days. FAD and SAD cortical NPCs showed indistinguishable culture morphology with healthy (control) NPCs (N = 5 per cell line). d and e No significant differences in NPC growth rates were identified (N = 4 per cell line, two-way Kruskal–Wallis P = NS). fn IPS-derived NPCs from healthy (control), FAD and SAD patients were assessed for canonical marker expression. Progenitor cells formed polarised rosettes expressing nestin (green; fh), PAX6 (red; ik) and SOX1 (green, ln). o No significant difference in nestin+ cells was observed between healthy and AD cell lines (N = 4 per cell line, ANOVA, F(2,9) = 0.022, P = NS). pr Under terminal neuronal differentiation conditions for 35–40 days, all patient samples showed positive expression of the neural marker β-III-tubulin (green). s No significant difference in the proportion of β-III-tubulin+ neurones between any individual (N = 4 per group, ANOVA, F(2,9) = 0.128, P = NS). tv Expression of the mature deep-layer cortical neuronal marker, CTIP2 was observed throughout cultures from each patient (green). Scale bars, 50 μm

The correct version of Fig. 1 is:

This has been corrected in both the PDF and HTML versions of the Article.


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