ArticleJCI insight2019
Myelin repair stimulated by CNS-selective thyroid hormone action.
Article in JCI insight, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers, 1 of them a synthesis that pooled it.
What it found
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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
56 citing papers in PubMed, 1 synthesis or guideline pooled it, 104 citations in OpenAlex.
- Current status of neuroprotective and neuroregenerative strategies in multiple sclerosis: A systematic review.Multiple sclerosis (Houndmills, Basingstoke, England) · 2022Pooled it
- Spinal cord microglia exhibit a dysfunctional response to myelin damage.Journal of neuroimmunology · 2026Article
- Review
- Cholesterol Quantification in Brain and Spinal Cord During Development, Demyelination, and Remyelination.Molecules (Basel, Switzerland) · 2026Article
- Quantitative determination of longitudinal CNS cholesterol loss during myelin damage and repair.bioRxiv : the preprint server for biology · 2026Article
- Emerging Roles, Mechanisms, and Therapeutic Potential of Thyroid Hormones in Neurodegenerative Diseases: A Review.Brain sciences · 2026Review
- Temporal Dynamics of CNS Cholesterol Esters Correlate with Demyelination and Remyelination.ACS chemical neuroscience · 2026Article
- Temporal dynamics of CNS cholesterol esters correlate with demyelination and remyelination.bioRxiv : the preprint server for biology · 2025Article
- Central thyroid hormone receptor-beta: Sensitivity to alcohol and a role in regulating alcohol drinking.Hormones and behavior · 2025Article
- Review
- FBXW7 regulates MYRF levels to control myelin capacity and homeostasis in the adult central nervous system.Nature communications · 2025Article
- Reduced cholesterol alters the biophysical properties of repaired myelin.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2025Article
- Targeting SMOX Preserves Optic Nerve Myelin, Axonal Integrity, and Visual Function in Multiple Sclerosis.Biomolecules · 2025Article
- Incomplete remyelination via therapeutically enhanced oligodendrogenesis is sufficient to recover visual cortical function.Nature communications · 2025Article
- Oligodendrocytes and myelination: pioneering new frontiers in cognitive neuroscience.Frontiers in neuroscience · 2025Review
- Inhibition of macrophage inflammasome assembly and pyroptosis with GC-1 ameliorates acute lung injury.Theranostics · 2025Article
- Clinical features and prognosis of NMOSD patients with positive autoimmune antibodies.Frontiers in neurology · 2025Article
- Remyelination protects neurons from DLK-mediated neurodegeneration.Nature communications · 2024Article
- Article
- Remyelination protects neurons from DLK-mediated neurodegeneration.bioRxiv : the preprint server for biology · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
19 authors at 3 institutions in 1 country.
Funding
Abstract
Oligodendrocyte processes wrap axons to form neuroprotective myelin sheaths, and damage to myelin in disorders, such as multiple sclerosis (MS), leads to neurodegeneration and disability. There are currently no approved treatments for MS that stimulate myelin repair. During development, thyroid hormone (TH) promotes myelination through enhancing oligodendrocyte differentiation; however, TH itself is unsuitable as a remyelination therapy due to adverse systemic effects. This problem is overcome with selective TH agonists, sobetirome and a CNS-selective prodrug of sobetirome called Sob-AM2. We show here that TH and sobetirome stimulated remyelination in standard gliotoxin models of demyelination. We then utilized a genetic mouse model of demyelination and remyelination, in which we employed motor function tests, histology, and MRI to demonstrate that chronic treatment with sobetirome or Sob-AM2 leads to significant improvement in both clinical signs and remyelination. In contrast, chronic treatment with TH in this model inhibited the endogenous myelin repair and exacerbated disease. These results support the clinical investigation of selective CNS-penetrating TH agonists, but not TH, for myelin repair.
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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.