Department of Veterinary Medical Sciences, University of Bologna, Bologna, Italy.
J Neuroendocrinol. 2011 Sep;23(9):778-90. doi: 10.1111/j.1365-2826.2011.02181.x.
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.
髓鞘再生失败是多发性硬化症（MS）慢性进展的一个关键标志，MS 是人类最常见的脱髓鞘疾病，但目前其具体原因仍不清楚。已有研究表明，甲状腺激素给药可改善急性和慢性脱髓鞘疾病啮齿动物模型的临床病程、病理学和髓鞘再生。在本研究中，我们将这种治疗尝试应用于非人类灵长类动物 Callithrix Jacchus（狨猴）的实验性自身免疫性脑脊髓炎（EAE）模型中。我们的研究结果表明，三碘甲状腺原氨酸（T3）短疗程给药可通过形态学、免疫组织化学和分子生物学评估，将脱髓鞘/髓鞘再生平衡向髓鞘再生方向转移，并改善疾病的临床病程。我们还发现，患有严重疾病的动物表现出甲状腺功能减退和脊髓中脱碘酶和甲状腺激素受体 mRNA 表达的严重改变，而甲状腺激素治疗可完全纠正这些改变。因此，我们认为甲状腺激素治疗通过纠正甲状腺激素细胞效应器的功能障碍，改善了 EAE 狨猴的髓鞘形态。
