Abstract
Clinical and subclinical hypothyroidism are the most common hormonal dysfunctions during pregnancy. Insufficient maternal thyroid hormones (THs) in the early stages of pregnancy can lead to severe impairments in the development of the central nervous system because THs are critical to central nervous system development. In the fetus and after birth, THs participate in neurogenic processes, cell differentiation, neuronal activation, axonal growth, dendritic arborization, synaptogenesis and myelination. Although treatment is simple and effective, approximately 30% of pregnant women in Brazil with access to prenatal care have their first consultation after the first trimester of pregnancy, and any delay in diagnosis and resulting treatment delay may lead to cognitive impairment in children. This review summarizes the effects of clinical and subclinical hypothyroidism on fetal neurodevelopment, behavior and cognition in humans and rodents. Arch Endocrinol Metab. 2020;64(1):89-95.
Highlights
Thyroid hormones (THs) are essential for the development, growth and metabolism of all vertebrates from the embryonic period onward
In rats with Clinical hypothyroidism (CH) and subclinical hypothyroidism (SCH), the expression of Egr-1, Arc, Erk and Bndf in their offspring’s hippocampus was significantly decreased, and Ras-proximate-1 protein (RAP-1) levels were increased when compared to the offspring of euthyroid rats, this was more pronounced in the HC roup
The consequences for central nervous system (CNS) development and cognition caused by insufficient maternal THs in CH are well known in humans and have been established experimentally in rodents
Summary
Thyroid hormones (THs) are essential for the development, growth and metabolism of all vertebrates from the embryonic period onward. T3 is an active TH capable of binding to high affinity receptors located in the nucleus of its target cells, the thyroid receptors (TRs). T3 is a biologically active hormone and is fundamental for growth, differentiation, activity regulation and organ and tissue metabolism, even in adult life [1]. The fetal thyroid becomes fully functional in humans from the second trimester of gestation. The source of THs during the first trimester is, exclusively maternal, and changes in TH availability may cause complications during pregnancy and have a negative effect on neurodevelopment, including consequences for behavior and cognition [3]. Controversy still exists regarding whether subclinical hypothyroidism (SCH) impacts the neurodevelopment and cognition of offspring
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