The DOI matches its Crossref record; 234 of the 235 references it cites were found in a registry or an index.
Modeling Alzheimer’s disease with iPSC-derived brain cells
Open accessAbstract
Alzheimer's disease is a devastating neurodegenerative disorder with no cure. Countless promising therapeutics have shown efficacy in rodent Alzheimer's disease models yet failed to benefit human patients. While hope remains that earlier intervention with existing therapeutics will improve outcomes, it is becoming increasingly clear that new approaches to understand and combat the pathophysiology of Alzheimer's disease are needed. Human induced pluripotent stem cell (iPSC) technologies have changed the face of preclinical research and iPSC-derived cell types are being utilized to study an array of human conditions, including neurodegenerative disease. All major brain cell types can now be differentiated from iPSCs, while increasingly complex co-culture systems are being developed to facilitate neuroscience research. Many cellular functions perturbed in Alzheimer's disease can be recapitulated using iPSC-derived cells in vitro, and co-culture platforms are beginning to yield insights into the complex interactions that occur between brain cell types during neurodegeneration. Further, iPSC-based systems and genome editing tools will be critical in understanding the roles of the numerous new genes and mutations found to modify Alzheimer's disease risk in the past decade. While still in their relative infancy, these developing iPSC-based technologies hold considerable promise to push forward efforts to combat Alzheimer's disease and other neurodegenerative disorders.
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“A majority of AD risk genes identified through genome-wide association studies are highly expressed in microglia, the brain’s innate immune cells, suggesting a key role in microglial dysfunction (Kummer et al., 2021; Penney et al., 2020; Teipel et al., 2022).”
From A novel molecular class that recruits HDAC/MECP2 complexes to PU.1 motifs reduces neuroinflammation (2023) · cites this paper as Penney et al., 2020
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“Population genetics has revealed that AD risk variants are enriched in genes that are highly expressed in microglia (Penney et al., 2020).”
From A novel molecular class that recruits HDAC/MECP2 complexes to PU.1 motifs reduces neuroinflammation (2023) · cites this paper as Penney et al., 2020
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“While it is well documented that iPS cell systems can model aspects of AD pathology (Penney et al., 2020; Nelson et al., 2023)”
From APOE3 Christchurch modulates β-catenin/Wnt signaling in iPS cell-derived cerebral organoids from Alzheimer’s cases (2024) · cites this paper as Penney et al., 2020
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Meta-Analysis of 74,046 Individuals Identifies 11 New Susceptibility Loci for Alzheimer’s Disease
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Cai, Y., Song, W., Li, J., Jing, Y., Liang, C., Zhang, L., Zhang, X., Zhang, W., Liu, B., An, Y., et al. (2022) · Science China Life Sciences · doi:10.1007/s11427-022-2161-3 · Cited by 450
TLR4 Cross-Talk With NLRP3 Inflammasome and Complement Signaling Pathways in Alzheimer's Disease
Yang, J., Wise, L., & Fukuchi, K.-I. (2020) · Frontiers in Immunology · doi:10.3389/fimmu.2020.00724 · Cited by 387
The complexity of Alzheimer’s disease: an evolving puzzle
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Lipid accumulation induced by APOE4 impairs microglial surveillance of neuronal-network activity
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Self-citationProteomic landscape of Alzheimer’s Disease: novel insights into pathogenesis and biomarker discovery
Bai, B., Vanderwall, D., Li, Y., Wang, X., Poudel, S., Wang, H., Dey, K. K., Chen, P., Yang, K., & Peng, J. (2021) · Molecular Neurodegeneration · doi:10.1186/s13024-021-00474-z · Cited by 267
Metadata
- Authors
- Penney, J., Ralvenius, W. T., & Tsai, L.-H.
- Affiliations
- Massachusetts Institute of Technology (US)
- Corresponding author
- Tsai, Li-Huei
- Venue
- Molecular Psychiatry
- Published
- 2019-08-07
- Volume
- 25
- Issue
- 1
- Pages
- 148-167
- ISSN
- 1359-4184 (ISSN-L)
- 1476-5578
- PMC
- PMC6906186
- OpenAlex
- W2964627277
- Cited by
- 471
- References
- 235
- Citations by year
- 2026: 54 · 2025: 66 · 2024: 78 · 2023: 84 · 2022: 77 · 2021: 65 · 2020: 41 · 2019: 6
- FWCI
- 4.18
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Locations
- Molecular Psychiatry (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DSpace@MIT (Massachusetts Institute of Technology) (submittedVersion, cc-by-nc)
- IslandScholar (University of Prince Edward Island) (submittedVersion)
- Funders
- National Science Foundation
- Cure Alzheimer's Fund
- Robert A. and Renee E. Belfer Family Foundation
- Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung (177920)
- National Institutes of Health (NS051874)
- National Institute on Aging (RF1AG054012)
- National Institute of Neurological Disorders and Stroke (R37NS051874)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Pluripotent Stem Cells Research
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Keywords
- Alzheimer's disease, induced pluripotent stem cells, neurodegeneration, co-culture model, disease modeling, genome editing, Alzheimer's disease risk genes, preclinical research
- MeSH terms
- Alzheimer Disease, Brain, Cell Differentiation, Humans, Models, Biological, Neurons, Neurodegenerative Diseases, Induced Pluripotent Stem Cells
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