ReviewAging cell2019
Harnessing cellular aging in human stem cell models of amyotrophic lateral sclerosis.
Review in Aging cell, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
20 citing papers in PubMed.
- Non-genetic neuromodulation with graphene optoelectronic actuators for disease models, stem cell maturation, and biohybrid robotics.Nature communications · 2025Article
- Current aspects of targeting cellular senescence for the therapy of neurodegenerative diseases.Frontiers in aging neuroscience · 2025Review
- Decoding Neurodegeneration: A Review of Molecular Mechanisms and Therapeutic Advances in Alzheimer's, Parkinson's, and ALS.International journal of molecular sciences · 2024Review
- Potential use of iPSCs for disease modeling, drug screening, and cell-based therapy for Alzheimer's disease.Cellular & molecular biology letters · 2023Review
- Article
- In Vitro 3D Modeling of Neurodegenerative Diseases.Bioengineering (Basel, Switzerland) · 2023Review
- Brain Regional Identity and Cell Type Specificity Landscape of Human Cortical Organoid Models.International journal of molecular sciences · 2022Article
- Human stem cell models of neurodegeneration: From basic science of amyotrophic lateral sclerosis to clinical translation.Cell stem cell · 2022Review
- Phenotyping Neurodegeneration in Human iPSCs.Annual review of biomedical data science · 2021Review
- Astrocytes and microglia in neurodegenerative diseases: Lessons from human in vitro models.Progress in neurobiology · 2021Review
- Reactive astrocytes in ALS display diminished intron retention.Nucleic acids research · 2021Article
- Genome Editing in iPSC-Based Neural Systems: From Disease Models to Future Therapeutic Strategies.Frontiers in genome editing · 2021Review
- Direct Reprogramming of Fibroblasts to Astrocytes Using Small Molecules.Methods in molecular biology (Clifton, N.J.) · 2021Article
- Opportunities and Challenges in Stem Cell Aging.Advances in experimental medicine and biology · 2021Review
- Patient-Specific Cells for Modeling and Decoding Amyotrophic Lateral Sclerosis: Advances and Challenges.Stem cell reviews and reports · 2020Review
- Decoding the relationship between ageing and amyotrophic lateral sclerosis: a cellular perspective.Brain : a journal of neurology · 2020Review
- On-chip 3D neuromuscular model for drug screening and precision medicine in neuromuscular disease.Nature protocols · 2020Article
- From Multi-Omics Approaches to Precision Medicine in Amyotrophic Lateral Sclerosis.Frontiers in neuroscience · 2020Review
- Harnessing cellular aging in human stem cell models of amyotrophic lateral sclerosis.Aging cell · 2019Review
- Temporal Control of Axonal Transport: The Extreme Case of Organismal Ageing.Frontiers in cellular neuroscience · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
Amyotrophic lateral sclerosis (ALS) is a relentlessly progressive neurodegenerative condition that is invariably fatal, usually within 3 to 5 years of diagnosis. The etiology of ALS remains unresolved and no effective treatments exist. There is therefore a desperate and unmet need for discovery of disease mechanisms to guide novel therapeutic strategies. The single major risk factor for ALS is aging, yet the molecular consequences of cell type-specific aging remain understudied in this context. Induced pluripotent stem cells (iPSCs) have transformed the standard approach of examining human disease, generating unlimited numbers of disease-relevant cells from patients, enabling analysis of disease mechanisms and drug screening. However, reprogramming patient cells to iPSCs reverses key hallmarks of cellular age. Therefore, although iPSC models recapitulate some disease hallmarks, a crucial challenge is to address the disparity between the advanced age of onset of neurodegenerative diseases and the fetal-equivalent maturational state of iPSC-derivatives. Increasing recognition of cell type-specific aging paradigms underscores the importance of heterogeneity in ultimately tipping the balance from a state of compensated dysfunction (clinically pre-symptomatic) to decompensation and progression (irreversible loss of neurological functions). In order to realize the true promise of iPSC technology in ALS, efforts need to prioritize faithfully recapitulating the clinical pathophysiological state, with proportionate emphasis on capturing the molecular sequelae of both cellular age and non-cell-autonomous disease mechanisms within this context.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.