APA
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Hartley, M. D., Banerji, T., Tagge, I., Kirkemo, L. L., Chaudhary, P., Calkins, E., … Scanlan, T. (2019). Myelin repair stimulated by CNS-selective thyroid hormone action. JCI Insight.
Chicago/Turabian
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Hartley, Meredith D., Tania Banerji, I. Tagge, Lisa L. Kirkemo, P. Chaudhary, E. Calkins, Danielle Galipeau, et al. “Myelin Repair Stimulated by CNS-Selective Thyroid Hormone Action.” JCI insight (2019).
MLA
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Hartley, Meredith D., et al. “Myelin Repair Stimulated by CNS-Selective Thyroid Hormone Action.” JCI Insight, 2019.
BibTeX Click to copy
@article{meredith2019a,
title = {Myelin repair stimulated by CNS-selective thyroid hormone action.},
year = {2019},
journal = {JCI insight},
author = {Hartley, Meredith D. and Banerji, Tania and Tagge, I. and Kirkemo, Lisa L. and Chaudhary, P. and Calkins, E. and Galipeau, Danielle and Shokat, Mitra and DeBell, Margaret J. and Leuven, Shelby Van and Miller, Hannah and Marracci, G. and Pocius, E. and Banerji, T. and Ferrara, S. and Meinig, J. M. and Emery, B. and Bourdette, D. and Scanlan, T.}
}
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.
