Hypothyroidism and Brain Development
Division of Anatomy and Embryology, Department of Zoology, Faculty of Science, Beni-Suef University, Beni-Suef, Egypt
- *Corresponding Author:
- Ahmed RG
Division of Anatomy and Embryology, Zoology Department
Faculty of Science, Beni-Suef University, Beni-Suef,Egypt
E-mail: [email protected]
Received date: July 25, 2017; Accepted date: August 22, 2017; Published date: August 25, 2017
Citation: Ahmed RG (2017) Hypothyroidism and Brain Development. J Anim Res Nutr Vol. 2 No. 2:13. doi: 10.21767/2572-5459.100033
Copyright: © 2017 Ahmed RG. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Letter to Editor
Thyroid hormones (THs) are central for the development of all biological systems Abalovich et al., El-bakry et al., Ahmed et al., Ahmed and Incerpi, Van Herck et al., Deepti et al., El-Ghareeb et al., Ahmed and El-Gareib and Caty et al. [1-4]. A moderate iodine deficiency causes maternal hypothyroxinemia, congenital hypothyroidism, preterm birth and mental retardation. Hypothyroidism during the development caused the following. Reduced the myelination of neuronal axons altered the dendritic structure cortical pyramidal cell [5-8]. Thompson and Potter reduced the Purkinje cell dendritic arborizations, the parallel fiber outgrowth and migration of the granule cells, and the number of granule cells diminished the synaptogenesis altered the molecular, morphological and functional actions of hippocampus and delayed the hypothalamic-pituitary development. Generally, THs deficiency during the early developmental period might delay the neuronal differentiation, decrease the neuronal connectivity, impair the motor skills and visual processing, and cause severe and permanent brain damage or mental retardation. Thus, these adverse effects may facilitate directly by a loss of the maternal THs contribution to the fetus or indirectly by the metabolic impairment of gestation, or both [9-12].
Conflict of Interest
The author declares that no competing financial interests exist.
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- Ahmed RG (2013) Early weaning PCB 95 exposure alters the neonatal endocrine system: thyroid adipokine dysfunction. J Endocrinol 219: 205-215.
- Ahmed RG (2014) Editorial: Do PCBs modify the thyroid-adipokine axis during development? Annals Thyroid Res 1: 11-12.
- Ahmed RG (2015) Chapter 1: Hypothyroidism and brain development. In Advances in Hypothyroidism Treatment. Avid Science Borsigstr. 9, 10115 Berlin, Berlin, Germany. Avid Science Publications level 6, Melange Towers, Wing a, Hitec City, Hyderabad, Telangana, India. 1-40.
- Ahmed RG (2015) Hypothyroidism and brain developmental players. Thyroid Research J 8: 1-12.
- Ahmed RG (2015) Editorials and Commentary: Maternofetal thyroid action and brain development. J adv biol 7: 1207-1213.
- Ahmed RG (2016) Gestational dexamethasone alters fetal neuroendocrine axis. Toxicology Letters 258: 46-54.
- Ahmed RG (2016) Neonatal polychlorinated biphenyls-induced endocrine dysfunction. Ann Thyroid. Res 2: 34-35.