Maternal Hypothyroidism and Multiple Sclerosis: Disruption the Developing Neuroendocrine System

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Maternalthyroid hormones (THs; 3,5,3’-triiodothyronine (T3) and thyroxin (T4)) have dynamic trophic actions during the perinatal development in particular the developing brain and myelination process. It is widely known that the appropriate myelinated growth, at postnatal day 25 in the rat, is responsible for protection and insulation of axons and is vital for the function of Central Nervous System (CNS), in particular the learning and memory function. Alternatively, there is a link between the hypothyroidism and the vulnerability of the CNS to inflammatory diseases by the thymus or spleen (cells of the immune system). In maternal hypothyroidism, the dysfunction in the thymic selection increases the accumulation of autoimmune T cells and the risk of autoimmune-inflammatory disorders in the offspring such as multiple sclerosis. Multiple sclerosis is a long-lasting, neuroinflammatory demyelinating dysfunction of the CNS that mostly disturbs young adults. The etiology of multiple sclerosis might be due to a disturbance in the genetic process, immunological (autoimmune disorders), infectious, or environmental factors. Symptoms of multiple sclerosis during pregnancy are urinary insistence, fatigue, lower extremities paresthesias and gait difficulties.

Onthe other hand, deficiency in the levels of maternal THs during the gestation can decrease the growth and differentiation of myelinated axons and cause permanent defects in the developing CNS including a mental retardation and cognitive disturbances. In mild-moderate iodine insufficiency, maternal and neonatal hypothyroxinemia, a low circulating free T4 with no change in free T3 or thyroid stimulating hormone (TSH), can disrupt the levels of nuclear Myelin Binding Protein (MBP) and increase the apoptosis causing a reduction in the cellular survival. More importantly, Wei et al. reported that hypothyroxinemia due to the maternal mild iodine decreases the expression of myelin-related proteins and delays the growth of neonatal myelination. Notably, a reduction in the levels of gestational THs can increase the severity of multiple sclerosis.