ArticleFrontiers in aging neuroscience2024
Modeling APOE ε4 familial Alzheimer's disease in directly converted 3D brain organoids.
Article in Frontiers in aging neuroscience, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Organoids: Key advances, optimization, and technological iterations in their application to neurodegenerative diseases.Neural regeneration research · 2026Article
- Brain organoids as precision models for neurodegenerative diseases: from disease modeling to drug discovery.Frontiers in neuroscience · 2026Review
- Modeling Alzheimer's disease with brain organoids: mechanisms, applications, and future directions.Frontiers in cell and developmental biology · 2026Review
- Catalpol promotes the generation of cerebral organoids with oRGs through activation of STAT3 signaling.Bioengineering & translational medicine · 2025Article
- Parkinson's Disease Modeling Using Directly Converted 3D Induced Dopaminergic Neuron Organoids and Assembloids.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- The translational power of Alzheimer's-based organoid models in personalized medicine: an integrated biological and digital approach embodying patient clinical history.Frontiers in cellular neuroscience · 2025Review
- Epigenetic Dynamics in Reprogramming to Dopaminergic Neurons for Parkinson's Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
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Authors and funding
7 authors.
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Abstract
Brain organoids have become a valuable tool for studying human brain development, disease modeling, and drug testing. However, generating brain organoids with mature neurons is time-intensive and often incomplete, limiting their utility in studying age-related neurodegenerative diseases such as Alzheimer's disease (AD). Here, we report the generation of 3D brain organoids from human fibroblasts through direct reprogramming, with simplicity, efficiency, and reduced variability. We also demonstrate that induced brain organoids from APOE ε4 AD patient fibroblasts capture some disease-specific features and pathologies associated with APOE ε4 AD. Moreover, APOE ε4-induced brain organoids with mutant APP overexpression faithfully recapitulate the acceleration of AD-related pathologies, providing a more physiologically relevant and patient-specific model of familial AD. Importantly, transcriptome analysis reveals that gene sets specific to APOE ε4 patient-induced brain organoids are highly similar to those of APOE ε4 post-mortem AD brains. Overall, induced brain organoids from direct reprogramming offer a promising approach for more efficient and controlled studies of neurodegenerative disease modeling.
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