Human iPSC-based modeling of late-onset disease via progerin-induced aging
Open accessAbstract
Reprogramming somatic cells to induced pluripotent stem cells (iPSCs) resets their identity back to an embryonic age and, thus, presents a significant hurdle for modeling late-onset disorders. In this study, we describe a strategy for inducing aging-related features in human iPSC-derived lineages and apply it to the modeling of Parkinson's disease (PD). Our approach involves expression of progerin, a truncated form of lamin A associated with premature aging. We found that expression of progerin in iPSC-derived fibroblasts and neurons induces multiple aging-related markers and characteristics, including dopamine-specific phenotypes such as neuromelanin accumulation. Induced aging in PD iPSC-derived dopamine neurons revealed disease phenotypes that require both aging and genetic susceptibility, such as pronounced dendrite degeneration, progressive loss of tyrosine hydroxylase (TH) expression, and enlarged mitochondria or Lewy-body-precursor inclusions. Thus, our study suggests that progerin-induced aging can be used to reveal late-onset age-related disease features in hiPSC-based disease models.
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Induction of pluripotency in iPSCs resets the age signatures of the donor cells to a fetal stage.
“However, induction of pluripotency in iPSCs resets the age signatures of the donor cells to a fetal stage (7–9).”
From Modeling late-onset Alzheimer’s disease neuropathology via direct neuronal reprogramming (2024) · cites this paper as [8]
The Results section, “Reprogramming reverts Age-Associated Markers to a ‘Young’ State,” reports that iPSCs from old donors lacked age-associated markers and resembled young-donor iPSCs. It does not establish that their age signatures were reset specifically to a fetal stage, and it notes that selection of cells with low marker expression cannot be ruled out. (LLM, conf=0.86)
Experimental — accuracy not yet measuredErasure of aging signatures and re-gaining of fetal identity represents a potent rescue in this study.
“Cellular aging features (Huh et al., 2016; Mertens et al., 2015a, 2018; Tang et al., 2017; Victor et al., 2014) and adult-like neuronal identity of iNs (Luo et al., 2019) are likely critical for the emergence of such phenotypes in sporadic AD neurons, because erasure of aging signatures and re-gaining of fetal identity represents a potent rescue in this study (Miller et al., 2013; Ocampo et al., 2”
From Age-dependent instability of mature neuronal fate in induced neurons from Alzheimer’s patients (2021) · cites this paper as Miller et al., 2013
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- Authors
- Miller, J. D., Ganat, Y. M., Kishinevsky, S., Bowman, R. L., Liu, B., Tu, E. Y., Mandal, P. K., Vera, E., Shim, J.-W., Kriks, S., Taldone, T., Fusaki, N., Tomishima, M. J., Krainc, D., Milner, T. A., Rossi, D. J., & Studer, L.
- Affiliations
- Memorial Sloan Kettering Cancer Center (US)
- Boston Children's Hospital (US)
- Keio University (JP)
- Harvard University (US)
- Weill Cornell Medicine (US)
- Corresponding author
- Studer, Lorenz
- ORCID
- Venue
- Cell stem cell
- Publisher
- Elsevier BV
- Published
- 2013-12
- Volume
- 13
- Issue
- 6
- Pages
- 691-705
- ISSN
- 1875-9777 (ISSN-L)
- 1934-5909
- PMC
- PMC4153390
- OpenAlex
- W2081914422
- Cited by
- 777
- References
- 291
- Citations by year
- 2026: 46 · 2025: 41 · 2024: 52 · 2023: 54 · 2022: 50 · 2021: 71 · 2020: 66 · 2019: 64 · 2018: 76 · 2017: 72 · 2016: 94 · 2015: 52 · 2014: 38 · 2013: 1
- FWCI
- 27.60
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell stem cell (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Science Foundation
- New York Stem Cell Foundation
- Memorial Sloan-Kettering Cancer Center
- National Institutes of Health
- National Heart, Lung, and Blood Institute (HL-098351, R01HL098351)
- National Institute on Drug Abuse (R01DA008259, DA08259)
- National Cancer Institute (F31CA167863, P30CA008748)
- National Institute of Neurological Disorders and Stroke (NS078338, U24NS078338, R01NS052671, R01NS076054, NS076054)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Pluripotent Stem Cells Research
- Health Sciences › Medicine › Neurology › Parkinson's Disease Mechanisms and Treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Keywords
- progerin, lamin A, premature aging, induced pluripotent stem cells, Parkinson's disease, late-onset disease, iPSC-derived fibroblasts, dendrite degeneration, tyrosine hydroxylase, Lewy bodies, mitochondrial enlargement, disease modeling
- MeSH terms
- Adult, Aged, Aged, 80 and over, Aging, Animals, Cell Differentiation, Child, Fibroblasts, Humans, Mesencephalon, Middle Aged, Models, Biological, Nuclear Proteins, Parkinson Disease, Phenotype, Protein Precursors, Tissue Donors, Biomarkers, Cellular Senescence, Age of Onset, Lamin Type A, Mice, Induced Pluripotent Stem Cells, Dopaminergic Neurons, Cellular Reprogramming
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