Journal Club: Friday December 9, 2011

Saturday, December 10, 2011

Raihan Faroqui (Tisch MS) presented the following article in Journal Club.

Article title:  Triiodothyronine Administration Ameliorates the Demyelination/Remyelination Ratio in a Non-Human Primate Model of Multiple Sclerosis by Correcting Tissue Hypothyroidism

Reference: G. D’Intino1,L. Lorenzini1,M. Fernandez, A. Taglioni, G. Perretta, G. Del Vecchio, P. Villoslada, L. Giardino and L. Calza. Journal of Neuroendocrinology. 2011. 23, 778–790.

Although remyelination of demyelinated lesions through the maturation of oligodendrocyte progenitor cells (OPCs) is known to partially offset the damage of the early, inflammatory phases of multiple sclerosis, the lack of full repair and progressive diminution of remyelinating capabilities – believed to be caused by some malfunction in the growth of OPCs or the neural progenitors from which they differentiate – is among the more frustrating features of the clinical course of MS as well as an apt target for research and treatment strategy. It is known that developmental myelination is a thyroid hormone-dependent process and that thyroid hormone improves remyelination in animal models of demyelinating disease. Consequently, the authors of the present study experimented with administration of triiodothyronine (T3), the active form of thyroid hormone, as treatment for experimental allergic encephalomyelitis (EAE) that had been induced in a group of marmosets (selected for their close resemblance to the clinical course of MS in humans). They also monitored levels of T3 and T4 (thyroid prohormone) in EAE-treated, EAE-untreated, and control animals. It was found that T3 treatment significantly improved both the clinical outcome of EAE animals and forestalled demyelination – though whether this was due to increased remyelination or greater conservation and protection of existing myelin sheath is difficult to discern – with untreated animals experiencing advanced disability in far greater numbers than treated animals. In addition, T3 treatment seemed to restore thyroid hormones and overall thyroid function to the level of control animals without inducing hyperthyroidism, while EAE-untreated animals experienced significant hypothyroidism. Further study is warranted but these results are promising for the use of T3 in addressing the OPC-maturation dysfunction in demyelinating disease in combination with stem cells and other emerging treatments.  

 

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