ArticleJournal of neurotrauma2025
A Model of Traumatic Brain Injury Oligomerizes Tau in Cortical Organoids and Induces Clinically Relevant Pathologies that Synergize with
Article in Journal of neurotrauma, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Translational benchmarking of 3D in vitro models of traumatic brain injury.Trends in biotechnology · 2026Review
- Integrated Necroptosis Within Programmed Cell Death in Traumatic Brain Injury.Molecular neurobiology · 2026Review
- Mechanical Stretch Disrupts Calcium Dynamics and Redistributes Piezo1 in Human Astrocytes.Annals of biomedical engineering · 2026Article
- Tau Oligomers Induce Brain Endothelial Cell Hyperpermeability and Increase NLRP3 Inflammasome Signaling and MMP-9 Activity.Microcirculation (New York, N.Y. : 1994) · 2026Article
- Multiscale 3D microfluidic platform for intraorganoid delivery.Research square · 2026Article
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
Traumatic brain injury (TBI) is the most important environmental risk factor for neurodegenerative disease. Tauopathy plays an important role in post-traumatic neurodegeneration. Human-induced pluripotent stem cell (hiPSC)-derived cortical organoids have exciting potential to reveal the influence of genotype on post-traumatic neurodegeneration because they permit manipulation of the genome in a human system. This study established an isogenic 3D cortical organoid model of TBI to investigate tau pathology and other clinically relevant injury phenotypes. Organoids generated from patient-derived hiPSC lines carrying the V337M or IVS10 + 16 Microtubule associated protein tau (
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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.