Journal
JOURNAL OF NEUROIMMUNOLOGY
Volume 352, Issue -, Pages -Publisher
ELSEVIER
DOI: 10.1016/j.jneuroim.2020.577468
Keywords
EAE; Thyromimetics; Oligodendrocytes; Myelin; Inflammation
Categories
Funding
- National Multiple Sclerosis Society [RG 5199A4, RG-1607-25053, RG 5106A1/1]
- Race to Erase MS
- OHSU Laura Fund for Innovation in Multiple Sclerosis
- NIH [DK52798, P30 NS061800]
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The study demonstrated that thyromimetics could prevent myelin and axonal degeneration in experimental autoimmune encephalomyelitis, reduce clinical disease symptoms, and protect oligodendrocytes against cell death.
We have previously demonstrated that thyromimetics stimulate oligodendrocyte precursor cell differentiation and promote remyelination in murine demyelination models. We investigated whether a thyroid receptor-beta selective thyromimetic, sobetirome (Sob), and its CNS-targeted prodrug, Sob-AM2, could prevent myelin and axonal degeneration in experimental autoimmune encephalomyelitis (EAE). Compared to controls, EAE mice receiving triiodothyronine (T3, 0.4 mg/kg), Sob (5 mg/kg) or Sob-AM2 (5 mg/kg) had reduced clinical disease and, within the spinal cord, less tissue damage, more normally myelinated axons, fewer degenerating axons and more oligodendrocytes. T3 and Sob also protected cultured oligodendrocytes against cell death. Thyromimetics thus might protect against oligodendrocyte death, demyelination and axonal degeneration as well as stimulate remyelination in multiple sclerosis.
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