Thyroid Hormone Disruption and Neurodevelopment

  • Noriyuki Koibuchi
  • Paul M. Yen

Part of the Contemporary Clinical Neuroscience book series (CCNE)

Table of contents

  1. Front Matter
    Pages i-viii
  2. Disruption of Thyroid Hormone Action at Molecular Level

    1. Front Matter
      Pages 1-1
    2. Rohit Anthony Sinha, Paul M. Yen
      Pages 3-21
    3. Masami Murakami
      Pages 23-31
    4. Kingsley Ibhazehiebo, Toshiharu Iwasaki, Noriyuki Koibuchi
      Pages 33-49
  3. Animal Models to Study Thyroid Hormone Disruption on Neurodevelopment

  4. Thyroid Hormone Disruption and Neurodevelopment: Human Studies

    1. Front Matter
      Pages 151-151
    2. Takehiro Suzuki, Takaaki Abe
      Pages 169-182
    3. Irene Campi, Paolo Beck-Peccoz
      Pages 183-204
  5. Back Matter
    Pages 205-209

About this book

Introduction

Thyroid hormone plays an important role in development and functional maintenance in the central nervous system.  Deficiency of thyroid hormone during fetal and early postnatal life induces abnormal development known as cretinism in humans.  However, the molecular mechanism of thyroid hormone action has not yet been fully understood.  Thyroid hormone action in the brain may be disrupted under various pathological conditions.  In addition, environmental factors including endocrine-disrupting chemicals and bacterial endotoxins may disrupt thyroid hormone action in brain, causing abnormal brain development and functional disruption.   This is a first book to comprehensively describe the effect of thyroid hormone disruption in the central nervous system.  The first section deals with the disruption of thyroid hormone action at the molecular level.  First the authors provide a summary of the possible molecular mechanisms of thyroid hormone action in the brain, then they discuss several factors that may disrupt thyroid hormone action. In the second section, animal models to study thyroid hormone action will be introduced.  An interesting character of thyroid hormone deficiency is that, without thyroid hormone, the thyroid hormone receptor may act as a “repressor” of gene expression, causing more severe consequence than those of thyroid hormone receptor knockout animals.  Thus, several different kind of animal models may be used to clarify the role of thyroid hormone and its receptor in the brain. In the third section, human studies on thyroid disease and neurodevelopment will be introduced.  Although endemic cretinism induced by iodine deficiency and sporadic cretinism by various thyroid mutation are well known, the pathophysiological mechanisms that create each abnormal phenotype are not fully understood.  ​

Keywords

brain development gene mutation hypothyroidism iodine thyroid hormone

Editors and affiliations

  • Noriyuki Koibuchi
    • 1
  • Paul M. Yen
    • 2
  1. 1.Department of Integrative PhysiologyGunma University Graduate School of MedicineMaebashiJapan
  2. 2.Laboratory of Hormonal Regulation Cardiovascular and Metabolic Disorders ProgramDuke-NUS Graduate Medical SchoolSingaporeSingapore

Bibliographic information

  • DOI https://doi.org/10.1007/978-1-4939-3737-0
  • Copyright Information Springer Science+Business Media New York 2016
  • Publisher Name Springer, New York, NY
  • eBook Packages Biomedical and Life Sciences
  • Print ISBN 978-1-4939-3735-6
  • Online ISBN 978-1-4939-3737-0
  • About this book
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