Trial reportThe Journal of neuroscience : the official journal of the Society for Neuroscience2013
Treatment with thyroxine restores myelination and clinical recovery after intraventricular hemorrhage.
Trial report in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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The trial behind it
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Who cites it
35 citing papers in PubMed, 66 citations in OpenAlex.
- Trial
- Emerging Roles, Mechanisms, and Therapeutic Potential of Thyroid Hormones in Neurodegenerative Diseases: A Review.Brain sciences · 2026Review
- Shh activation restores interneurons and cognitive function in newborns with intraventricular haemorrhage.Brain : a journal of neurology · 2023Article
- Preserving and enhancing mitochondrial function after stroke to protect and repair the neurovascular unit: novel opportunities for nanoparticle-based drug delivery.Frontiers in cellular neuroscience · 2023Review
- Severe intraventricular hemorrhage causes long-lasting structural damage in a preterm rabbit pup model.Pediatric research · 2022Article
- SECISBP2L-Mediated Selenoprotein Synthesis Is Essential for Autonomous Regulation of Oligodendrocyte Differentiation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- Recovery of the brain after intraventricular hemorrhage.Seminars in fetal & neonatal medicine · 2022Review
- Thyroid hormone-dependent oligodendroglial cell lineage genomic and non-genomic signaling through integrin receptors.Frontiers in pharmacology · 2022Review
- PPAR-γ activation enhances myelination and neurological recovery in premature rabbits with intraventricular hemorrhage.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- White matter injury in infants with intraventricular haemorrhage: mechanisms and therapies.Nature reviews. Neurology · 2021Review
- Thyroid hormone deficiency during zebrafish development impairs central nervous system myelination.PloS one · 2021Article
- Human Cord Blood-Derived Unrestricted Somatic Stem Cell Infusion Improves Neurobehavioral Outcome in a Rabbit Model of Intraventricular Hemorrhage.Stem cells translational medicine · 2019Article
- Paradigms of Dynamic Control of Thyroid Hormone Signaling.Endocrine reviews · 2019Review
- GSK3β Inhibition Restores Impaired Neurogenesis in Preterm Neonates With Intraventricular Hemorrhage.Cerebral cortex (New York, N.Y. : 1991) · 2019Article
- Antenatal prevention of cerebral palsy and childhood disability: is the impossible possible?The Journal of physiology · 2018Review
- Glycogen synthase kinase-3β inhibition enhances myelination in preterm newborns with intraventricular hemorrhage, but not recombinant Wnt3A.Neurobiology of disease · 2018Article
- White matter injury in the preterm infant: pathology and mechanisms.Acta neuropathologica · 2017Review
- Pharmacological approaches to intervention in hypomyelinating and demyelinating white matter pathology.Neuropharmacology · 2016Review
- Thyroid Hormone Signaling in Oligodendrocytes: from Extracellular Transport to Intracellular Signal.Molecular neurobiology · 2016Review
- Combination of endogenous neural stem cell mobilization and lithium chloride treatment for hydrocephalus following intraventricular hemorrhage.Experimental and therapeutic medicine · 2016Article
Corrections and comments
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Authors and funding
14 authors at 7 institutions in 1 country.
Funding
Abstract
Intraventricular hemorrhage (IVH) remains a major cause of white matter injury in preterm infants with no viable therapeutic strategy to restore myelination. Maturation of oligodendrocytes and myelination is influenced by thyroid hormone (TH) signaling, which is mediated by TH receptor α (TRα) and TRβ. In the brain, cellular levels of TH are regulated by deiodinases, with deiodinase-2 mediating TH activation and deiodinase-3 TH inactivation. Therefore, we hypothesized that IVH would decrease TH signaling via changes in the expression of deiodinases and/or TRs, and normalization of TH signaling would enhance maturation of oligodendrocytes and myelination in preterm infants with IVH. These hypotheses were tested using both autopsy materials from human preterm infants and a rabbit model of IVH. We found that deiodinase-2 levels were reduced, whereas deiodinase-3 levels were increased in brain samples of both humans and rabbits with IVH compared with controls without IVH. TRα expression was also increased in human infants with IVH. Importantly, treatment with TH accelerated the proliferation and maturation of oligodendrocytes, increased transcription of Olig2 and Sox10 genes, augmented myelination, and restored neurological function in pups with IVH. Consistent with these findings, the density of myelinating oligodendrocytes was almost doubled in TH-treated human preterm infants compared with controls. Thus, in infants with IVH the combined elevation in deiodinase-3 and reduction in deiodinase-2 decreases TH signaling that can be worsened by an increase in unliganded TRα. Given that TH promotes neurological recovery in IVH, TH treatment might improve the neurodevelopmental outcome of preterm infants with IVH.
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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.