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Role of thyroid hormones in normal and abnormal central nervous system myelination in humans and rodents

期刊

FRONTIERS IN NEUROENDOCRINOLOGY
卷 61, 期 -, 页码 -

出版社

ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.yfrne.2021.100901

关键词

Allan-Herndon-Dudley syndrome; Hypothyroidism; Intrauterine growth restriction; Monocarboxylate transporter 8; Multiple sclerosis; Myelin; Oligodendrocytes; Thyromimetics; Transthyretin; White matter

资金

  1. Australian Research Council Future Fellowship [FT180100082]
  2. National Health and Medical Research Council [APP1161466]
  3. Research Foundation, Cerebral Palsy Alliance [PG216]
  4. Australian Research Council [FT180100082] Funding Source: Australian Research Council

向作者/读者索取更多资源

Thyroid hormones play a crucial role in vertebrate central nervous system development and function, particularly in the key neurodevelopmental process of myelination. Adequate levels of THs are essential for promoting proper neural function by supporting the maturation of myelin-producing cells.
Thyroid hormones (THs) are instrumental in promoting the molecular mechanisms which underlie the complex nature of neural development and function within the central nervous system (CNS) in vertebrates. The key neurodevelopmental process of myelination is conserved between humans and rodents, of which both experience peak fetal TH concentrations concomitant with onset of myelination. The importance of supplying adequate levels of THs to the myelin producing cells, the oligodendrocytes, for promoting their maturation is crucial for proper neural function. In this review we examine the key TH distributor and transport proteins, including transthyretin (TTR) and monocarboxylate transporter 8 (MCT8), essential for supporting proper oligodendrocyte and myelin health; and discuss disorders with impaired TH signalling in relation to abnormal CNS myelination in humans and rodents. Furthermore, we explore the importance of using novel TH analogues in the treatment of myelination disorders associated with abnormal TH signalling.

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