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Books > Science & Mathematics > Biology, life sciences > Life sciences: general issues > Neurosciences
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Thyroid Hormone Disruption and Neurodevelopment (Hardcover, 1st ed. 2017)
Loot Price: R5,690
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Thyroid Hormone Disruption and Neurodevelopment (Hardcover, 1st ed. 2017)
Series: Contemporary Clinical Neuroscience
Expected to ship within 12 - 19 working days
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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.
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