ArticleCell death & disease2017
Aberrant iPSC-derived human astrocytes in Alzheimer's disease.
Article in Cell death & disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 100 papers.
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Who cites it
100 citing papers in PubMed.
- Written in the Stars: Astrocyte Biology From Evolution to Disease.Acta physiologica (Oxford, England) · 2026Review
- MicroRNA and Alzheimer's disease: Diagnostic biomarkers and potential therapeutic targets.Neural regeneration research · 2026Article
- Glial and Neuronal Alzheimer's Disease-Related Alterations Reproduced in Human Induced Pluripotent Stem Cells With Presenilin-1 Mutation.Research square · 2026Article
- Modeling neurovascular dysfunction in Alzheimer's disease using an isogenic brain-chip model.Fluids and barriers of the CNS · 2026Article
- Development of Patient-Derived Neuroprogenitor Cells (hNPCs), Neurons and Astrocytes to Explore the Etiology of Guam Parkinsonism-Dementia Complex (PDC).bioRxiv : the preprint server for biology · 2025Article
- Presenilin 1 E280A mutation induces dysfunctional astrocytic phenotype in menstrual stromal-derived astrocyte-like cells.Cellular and molecular life sciences : CMLS · 2025Article
- In reply to Letter to the Editor from Paudel: Comment on "Changes in iPSC-Astrocyte Morphology Reflect Alzheimer's Disease Patient Clinical Markers".Stem cells (Dayton, Ohio) · 2025Article
- Comment on "Changes in iPSC-Astrocyte Morphology Reflect Alzheimer's Disease Patient Clinical Markers".Stem cells (Dayton, Ohio) · 2025Article
- Neural Metabolic Networks: Key Elements of Healthy Brain Function.Journal of neurochemistry · 2025Review
- Current Development of iPSC-Based Modeling in Neurodegenerative Diseases.International journal of molecular sciences · 2025Review
- Fueling Brain Inhibition: Integrating GABAergic Neurotransmission and Energy Metabolism.Neurochemical research · 2025Review
- Increasing hexokinase 1 expression improves mitochondrial and glycolytic functional deficits seen in sporadic Alzheimer's disease astrocytes.Molecular psychiatry · 2025Article
- The Glutamate/GABA-Glutamine Cycle: Insights, Updates, and Advances.Journal of neurochemistry · 2025Review
- Altered metabolic function induced by Aβ-oligomers and PSEN1 mutations in iPSC-derived astrocytes.Journal of neurochemistry · 2025Article
- Advancing Alzheimer's Disease Modelling by Developing a Refined Biomimetic Brain Microenvironment for Facilitating High-Throughput Screening of Pharmacological Treatment Strategies.International journal of molecular sciences · 2024Review
- Primary cortical cell tri-culture to study effects of amyloid-β on microglia function and neuroinflammatory response.Journal of Alzheimer's disease : JAD · 2024Article
- Assessment and Evaluation of Contemporary Approaches for Astrocyte Differentiation from hiPSCs: A Modeling Paradigm for Alzheimer's Disease.Biological procedures online · 2024Article
- PRDM16-DT is a novel lncRNA that regulates astrocyte function in Alzheimer's disease.Acta neuropathologica · 2024Article
- Inflammatory aspects of Alzheimer's disease.Acta neuropathologica · 2024Review
- PRDM16-DT: A Brain and Astrocyte-Specific lncRNA Implicated in Alzheimer's Disease.bioRxiv : the preprint server for biology · 2024Article
40 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
4 authors.
Funding
Abstract
The pathological potential of human astroglia in Alzheimer's disease (AD) was analysed in vitro using induced pluripotent stem cell (iPSC) technology. Here, we report development of a human iPSC-derived astrocyte model created from healthy individuals and patients with either early-onset familial AD (FAD) or the late-onset sporadic form of AD (SAD). Our chemically defined and highly efficient model provides >95% homogeneous populations of human astrocytes within 30 days of differentiation from cortical neural progenitor cells (NPCs). All astrocytes expressed functional markers including glial fibrillary acidic protein (GFAP), excitatory amino acid transporter-1 (EAAT1), S100B and glutamine synthetase (GS) comparable to that of adult astrocytes in vivo. However, induced astrocytes derived from both SAD and FAD patients exhibit a pronounced pathological phenotype, with a significantly less complex morphological appearance, overall atrophic profiles and abnormal localisation of key functional astroglial markers. Furthermore, NPCs derived from identical patients did not show any differences, therefore, validating that remodelled astroglia are not as a result of defective neural intermediates. This work not only presents a novel model to study the mechanisms of human astrocytes in vitro, but also provides an ideal platform for further interrogation of early astroglial cell autonomous events in AD and the possibility of identification of novel therapeutic targets for the treatment of AD.
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