PSEN1 Mutant iPSC-Derived Model Reveals Severe Astrocyte Pathology in Alzheimer's Disease
Open accessAbstract
Alzheimer's disease (AD) is a common neurodegenerative disorder and the leading cause of cognitive impairment. Due to insufficient understanding of the disease mechanisms, there are no efficient therapies for AD. Most studies have focused on neuronal cells, but astrocytes have also been suggested to contribute to AD pathology. We describe here the generation of functional astrocytes from induced pluripotent stem cells (iPSCs) derived from AD patients with PSEN1 ΔE9 mutation, as well as healthy and gene-corrected isogenic controls. AD astrocytes manifest hallmarks of disease pathology, including increased β-amyloid production, altered cytokine release, and dysregulated Ca 2+ homeostasis. Furthermore, due to altered metabolism, AD astrocytes show increased oxidative stress and reduced lactate secretion, as well as compromised neuronal supportive function, as evidenced by altering Ca 2+ transients in healthy neurons. Our results reveal an important role for astrocytes in AD pathology and highlight the strength of iPSC-derived models for brain diseases.
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The continuum of GFAP/S100B-positive cells, ranging from roundish/polarized to highly arborized cells, agrees with previous studies.
“In our study, the continuum of GFAF/S100B-positive cells, ranging from roundish/polarized ones to highly arborized cells, agrees with previous studies [27,28].”
From Emerging Role of miR-21-5p in Neuron–Glia Dysregulation and Exosome Transfer Using Multiple Models of Alzheimer’s Disease (2022) · cites this paper as [27]
The Results section, under “iPSCs Efficiently Differentiate into Functional Astrocytes” (page unavailable), reports GFAP- and/or S100β-positive cells acquiring a stellate morphology. It does not describe the claimed continuum from roundish or polarized to highly arborized cells. (LLM, conf=0.82)
Experimental — accuracy not yet measuredAst-AD revealed fewer GFAP-positive cells than S100B-positive ones, with low HMGB1 and IL-10 and elevated IL-6 and C/EBPα gene levels.
“Ast-AD revealed fewer GFAP-positive cells than S100B-positive ones, with low HMGB1 and IL-10 and elevated IL-6 and C/EBPα gene levels, already pointing to some altered properties [27,72,120].”
From Emerging Role of miR-21-5p in Neuron–Glia Dysregulation and Exosome Transfer Using Multiple Models of Alzheimer’s Disease (2022) · cites this paper as [27]
The Results section on cytokine secretion (page unavailable) reports higher IL-6 and IL-10 secretion by stimulated PSEN1 ΔE9 astrocytes than controls, supporting altered IL-6 activity but not the claim of low IL-10 or elevated IL-6 gene levels in AD cells. The astrocyte-characterization Results (page unavailable) report GFAP and/or S100β staining, but not fewer GFAP-positive than S100β-positive AD cells. The retrieved passages do not report the claimed HMGB1 or C/EBPα gene levels. (LLM, conf=0.87)
Experimental — accuracy not yet measuredThe iPSC lines used were characterized for genetic stability and pluripotency markers.
“Characterization for genetic stability and pluripotency markers of these iPSCs was previously documented in studies using iPSC differentiation into astrocytes and microglia for the screening of AD-associated glial aberrancies [26,27].”
From Emerging Role of miR-21-5p in Neuron–Glia Dysregulation and Exosome Transfer Using Multiple Models of Alzheimer’s Disease (2022) · cites this paper as [27]
Ast cells displayed heterogeneous shapes, mostly stellate morphology, and expressed GFAP and S100B.
“The cells displayed heterogeneous shapes, but mostly the stellate morphology characteristic of glial cells [27] (Figure 6B), and the astrocyte-associated GFAP and S100B markers (Figure 6C)”
From Emerging Role of miR-21-5p in Neuron–Glia Dysregulation and Exosome Transfer Using Multiple Models of Alzheimer’s Disease (2022) · cites this paper as [27]
Some authors have stimulated astrocytes with TNF-α and IL-1β to make their pathological profiles more visible.
“some authors have stimulated astrocytes with TNF-α and IL-1β to make their pathological profiles more visible [27].”
From Emerging Role of miR-21-5p in Neuron–Glia Dysregulation and Exosome Transfer Using Multiple Models of Alzheimer’s Disease (2022) · cites this paper as [27]
Astrocytes contribute to neuroinflammation when reactive.
“because astrocytes are known to contribute to neuroinflammation when reactive”
From Emerging Role of miR-21-5p in Neuron–Glia Dysregulation and Exosome Transfer Using Multiple Models of Alzheimer’s Disease (2022) · cites this paper as [27]
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- Authors
- Oksanen, M., Petersen, A. J., Naumenko, N., Puttonen, K., Lehtonen, Š., Gubert Olivé, M., Shakirzyanova, A., Leskelä, S., Sarajärvi, T., Viitanen, M., Rinne, J. O., Hiltunen, M., Haapasalo, A., Giniatullin, R., Tavi, P., Zhang, S.-C., Kanninen, K. M., Hämäläinen, R. H., & Koistinaho, J.
- Affiliations
- University of Eastern Finland (FI)
- University of Wisconsin–Madison (US)
- Karolinska University Hospital (SE)
- University of Turku (FI)
- University of Wisconsin System (US)
- ORCID
- Venue
- Stem Cell Reports
- Publisher
- Elsevier BV
- Published
- 2017-12
- Volume
- 9
- Issue
- 6
- Pages
- 1885-1897
- ISSN
- 2213-6711 (ISSN-L)
- PMC
- PMC5785689
- OpenAlex
- W2768957663
- Cited by
- 332
- References
- 65
- Citations by year
- 2026: 27 · 2025: 22 · 2024: 46 · 2023: 37 · 2022: 49 · 2021: 41 · 2020: 50 · 2019: 43 · 2018: 17
- FWCI
- 22.27
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Stem Cell Reports (publishedVersion, cc-by-nc-nd)
- Europe PMC (PubMed Central) (publishedVersion, cc-by-nc-nd)
- PubMed Central (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- UEF eRepo (University of Eastern Finland) (submittedVersion, cc-by-nc-nd)
- UTUPub (University of Turku) (submittedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Itä-Suomen Yliopisto
- Academy of Finland
- Tekes
- Emil Aaltosen Säätiö
- Sigrid Juséliuksen Säätiö
- Horizon 2020 (643417)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Pluripotent Stem Cells Research
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- Alzheimer's disease, astrocytes, induced pluripotent stem cells, iPSC-derived astrocytes, amyloid-beta production, cytokine production, calcium homeostasis, oxidative stress, lactate secretion, disease modeling, isogenic controls
- MeSH terms
- Alzheimer Disease, Animals, Astrocytes, Brain, Calcium, Gene Expression Regulation, Humans, Mitochondria, Neurons, Amyloid beta-Peptides, Oxidative Stress, Lactic Acid, Presenilin-1, Induced Pluripotent Stem Cells
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
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