ArticleScience (New York, N.Y.)2024
Modeling late-onset Alzheimer's disease neuropathology via direct neuronal reprogramming.
Article in Science (New York, N.Y.), 2024. 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 47 papers.
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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.
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Who cites it
47 citing papers in PubMed.
- Direct neuronal reprogramming: emerging therapeutic strategies for neurodegenerative disorders.Annals of medicine · 2026Review
- Distinct media requirements for dopaminergic neuron reprogramming from human glia and fibroblasts.Scientific reports · 2026Article
- Cross-species functional analysis of aResearch square · 2026Article
- Development of a Novel AAV-Mediated microRNA Gene Therapy for Spatial Suppression of BACE1 to Improve Cognitive Function in Alzheimer's Disease Model Mice.Biomolecules · 2026Article
- Efficient chemical reprogramming of human T cells into functional megakaryocytes and platelets.Science advances · 2026Article
- Patient-derived tau-seeded human neuronal chimeras recapitulate mature Alzheimer's tau pathology and uncover human-specific neuronal vulnerability.bioRxiv : the preprint server for biology · 2026Article
- MicroRNA and Alzheimer's disease: Diagnostic biomarkers and potential therapeutic targets.Neural regeneration research · 2026Article
- Three-dimensional direct neuronal reprogramming for modeling Alzheimer's disease neuropathology.Nature protocols · 2026Review
- Emerging directions in tauopathy research.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Review
- A multimodal adaptive optical microscope for in vivo imaging from molecules to organisms.Nature methods · 2026Article
- Using iPSC models to examine neuron-glia interactions in neurodegenerative diseases.Bioscience reports · 2026Review
- Recapitulation of plaque formation, tau pathology, and neurodegeneration in a human 3D matrix model of Alzheimer's disease.Cell reports methods · 2026Article
- Transposable elements in the dark genome.Nature biotechnology · 2026Article
- Modeling Late-Onset Sporadic Alzheimer's Disease Using Patient-Derived Cells: A Review.Neurology international · 2026Review
- Prefoldin 5 is a microtubule-associated protein that suppresses Tau aggregation and neurotoxicity.eLife · 2026Article
- Methodology for human-induced pluripotent stem cell-derived excitatory and inhibitory neuron coculture with astrocytes for Alzheimer's disease modelling.Brain communications · 2026Article
- Modeling Alzheimer's disease with brain organoids: mechanisms, applications, and future directions.Frontiers in cell and developmental biology · 2026Review
- Molecular and cellular processes connecting type 2 diabetes to Alzheimer's disease, focusing on oxidative stress, metabolic dysfunction, and neurodegeneration.Genetics and molecular biology · 2026Article
- Direct neuronal reprogramming for neurological diseases: applications, translational Challenges, and future directions.Frontiers in neuroscience · 2026Review
- Epigenetic Changes in Alzheimer's Disease and Interventions for Therapy.Neuropsychiatric disease and treatment · 2026Review
Corrections and comments
- Erratum issued
- Update of
Authors and funding
21 authors.
Funding
Abstract
Late-onset Alzheimer's disease (LOAD) is the most common form of Alzheimer's disease (AD). However, modeling sporadic LOAD that endogenously captures hallmark neuronal pathologies such as amyloid-β (Aβ) deposition, tau tangles, and neuronal loss remains an unmet need. We demonstrate that neurons generated by microRNA (miRNA)-based direct reprogramming of fibroblasts from individuals affected by autosomal dominant AD (ADAD) and LOAD in a three-dimensional environment effectively recapitulate key neuropathological features of AD. Reprogrammed LOAD neurons exhibit Aβ-dependent neurodegeneration, and treatment with β- or γ-secretase inhibitors before (but not subsequent to) Aβ deposit formation mitigated neuronal death. Moreover inhibiting age-associated retrotransposable elements in LOAD neurons reduced both Aβ deposition and neurodegeneration. Our study underscores the efficacy of modeling late-onset neuropathology of LOAD through high-efficiency miRNA-based neuronal reprogramming.
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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.