Journal
JOURNAL OF NEUROENDOCRINOLOGY
Volume 23, Issue 9, Pages 778-790Publisher
WILEY
DOI: 10.1111/j.1365-2826.2011.02181.x
Keywords
thyroid hormone; marmoset; remyelination; oligodendrocyte precursor cells; experimental allergic encephalomyelitis
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Funding
- Regione Emilia Romagna
- PRRIITT projects
- Italian Multiple Sclerosis Foundation
- Centro di Fisiopatologia del Sistema Nervoso, Modena
- IRET-ONLUS Foundation, Bologna
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Remyelination failure is a key landmark in chronic progression of multiple sclerosis (MS), the most diffuse demyelinating disease in human, but the reasons for this are still unknown. It has been shown that thyroid hormone administration in the rodent models of acute and chronic demyelinating diseases improved their clinical course, pathology and remyelination. In the present study, we translated this therapeutic attempt to experimental allergic encephalomyelitis (EAE) in the non-human primate Callithrix Jacchus (marmoset). We report that short protocols of triiodothyronine treatment shifts the demyelination/remyelination balance toward remyelination, as assessed by morphology, immunohistochemistry and molecular biology, and improves the clinical course of the disease. We also found that severely ill animals display hypothyroidism and severe alteration of deiodinase and thyroid hormone receptor mRNAs expression in the spinal cord, which was completely corrected by thyroid hormone treatment. We therefore suggest that thyroid hormone treatment improves myelin sheath morphology in marmoset EAE, by correcting the dysfunction of thyroid hormone cellular effectors.
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