Thyroid hormones states and brain development interactions.
The action of thyroid hormones (THs) in the brain is strictly regulated, since these hormones play a crucial role in the development and physiological functioning of the central nervous system (CNS). Disorders of the thyroid gland are among the most common endocrine maladies. Therefore, the objective of this study was to identify in broad terms the interactions between thyroid hormone states or actions and brain development. THs regulate the neuronal cytoarchitecture, neuronal growth and synaptogenesis, and their receptors are widely distributed in the CNS. Any deficiency or increase of them (hypo- or hyperthyroidism) during these periods may result in an irreversible impairment, morphological and cytoarchitecture abnormalities, disorganization, maldevelopment and physical retardation. This includes abnormal neuronal proliferation, migration, decreased dendritic densities and dendritic arborizations. This drastic effect may be responsible for the loss of neurons vital functions and may lead, in turn, to the biochemical dysfunctions. This could explain the physiological and behavioral changes observed in the animals or human during thyroid dysfunction. It can be hypothesized that the sensitive to the thyroid hormones is not only remarked in the neonatal period but also prior to birth, and THs change during the development may lead to the brain damage if not corrected shortly after the birth. Thus, the hypothesis that neurodevelopmental abnormalities might be related to the thyroid hormones is plausible. Taken together, the alterations of neurotransmitters and disturbance in the GABA, adenosine and pro/antioxidant systems in CNS due to the thyroid dysfunction may retard the neurogenesis and CNS growth and the reverse is true. In general, THs disorder during early life may lead to distortions rather than synchronized shifts in the relative development of several central transmitter systems that leads to a multitude of irreversible morphological and biochemical abnormalities (pathophysiology). Thus, further studies need to be done to emphasize this concept.
Ahmed
Osama M
OM
Zoology Department, Faculty of Science, Beni Suef University, Egypt. ahmedragab790@yahoo.com
El-Gareib
A W
AW
El-Bakry
A M
AM
Abd El-Tawab
S M
SM
Ahmed
R G
RG
D000818:Animals; D001921:Brain / Q000002:abnormalities / Q000254:growth & development / Q000378:metabolism*; D001928:Brain Diseases, Metabolic / Q000378:metabolism* / Q000503:physiopathology; D002454:Cell Differentiation / Q000502:physiology; D002648:Child; D002658:Developmental Disabilities / Q000378:metabolism* / Q000503:physiopathology; D006801:Humans; D009421:Nervous System Malformations / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology; D009474:Neurons / Q000378:metabolism / Q000473:pathology; D013959:Thyroid Diseases / Q000150:complications / Q000378:metabolism* / Q000503:physiopathology; D013961:Thyroid Gland / Q000378:metabolism* / Q000503:physiopathology; D013963:Thyroid Hormones / Q000378:metabolism*
D013963:Thyroid Hormones