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Is neuropsychological development related to maternal hypothyroidism or to maternal hypothyroxinemia?
TLDR
It is proposed that the screening of pregnant women for thyroid disorders should include the determination of free T4 as soon as possible during the first trimester as a major test, because hypothyroxinemia has been related to poor developmental outcome, irrespective of the presence of high titers of thyroid autoantibodies or elevated serum TSH.
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Role of thyroid hormone during early brain development.
TLDR
The first trimester surge of maternal FT4 is proposed as a biologically relevant event controlled by the conceptus to ensure its developing cerebral cortex is provided with the necessary amounts of substrate for the local generation of adequate amounts of T3 for binding to its nuclear receptor.
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Making the gradient: thyroid hormone regulates cone opsin expression in the developing mouse retina.
TLDR
The results suggest that the ratio and patterning of cone types may be determined by TH availability during retinal development, and that a TH gradient may play a role in establishing the gradient of M-opsin.
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Early maternal hypothyroxinemia alters histogenesis and cerebral cortex cytoarchitecture of the progeny.
TLDR
This work believes that this is the first direct evidence of an alteration in fetal brain histogenesis and cytoarchitecture that could only be related to early maternal hypothyroxinemia, and ought to be prevented both by mass screening of free thyroxine in early pregnancy and by early iodine supplementation to avoid iodine deficiency, however mild.
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A moderate and transient deficiency of maternal thyroid function at the beginning of fetal neocorticogenesis alters neuronal migration.
TLDR
The experimental approach was designed to result in a mild and transient period of maternal hypothyroxinemia at the beginning of corticogenesis, and when extrapolated to man, these results stress the need for prevention of hypothyruinemia before midpregnancy, however moderate, and whichever the underlying cause.
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Fetal tissues are exposed to biologically relevant free thyroxine concentrations during early phases of development.
TLDR
It is found that in all fetal fluids the concentrations of T(4) available to developing tissues, namely FT(4), reach values that are at least one third of those biologically active in their euthyroid mothers.
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Iodothyronine levels in the human developing brain: major regulatory roles of iodothyronine deiodinases in different areas.
TLDR
The hypothesis that T(3) is required by the human cerebral cortex before midgestation, when mother is the only source of T(4) is supported, and D3 protects brain regions from excessive T( 3) until differentiation is required.
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Regulation of Iodothyronine Deiodinase Activity as Studied in Thyroidectomized Rats Infused with Thyroxine or Triiodothyronine.
To provide new insights into the in vivo regulation of iodothyronine deiodinases in the different tissues of the rat, we have evaluated the effects on these enzymatic activities of T4 or T3 infusions…
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Role of Late Maternal Thyroid Hormones in Cerebral Cortex Development: An Experimental Model for Human Prematurity
TLDR
Maternal THs are still essential for normal offspring's neurodevelopment even after onset of fetal thyroid function and the data suggest that thyroxine treatment of premature neonates should be attempted to compensate for the interruption of the maternal supply.
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Corticotropin-releasing factor stimulates metamorphosis and increases thyroid hormone concentration in prometamorphic Rana perezi larvae.
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