The link between thyroid hormone deficiency and optimal neurodevelopment in early childhood is well established. More recently, data from animal model experiments and epidemiological databases have indicated that perturbations in maternal and fetal thyroid hormone concentrations may affect fetal outcome and, in particular, have an adverse effect on neurodevelopmental outcome. Epidemiological evidence in human pregnancies has indicated that hypothyroxinaemia in the fetus in the first and early second trimester (if sustained) may cause a significant measurable drop in developmental quotient as the child develops throughout infancy.
Delivery of thyroid hormone to the neurons comprising of the central nervous system in the fetus is dependent upon maternal thyroid hormone concentrations, transplacental passage of maternal thyroid hormone, circulating fetal thyroid hormone concentrations and the local release of active thyroid hormone at or within the fetal neuron.
Such a homeostatic process relies on an intact maternal and fetal thyroid gland but also the expression and post-translational activation of thyroid hormone receptors upon target cells and also a sub-group of deiodinases (3 common sub-types) to release the active ligand, tri-iodothyrine (T3) to the neurone.
Our group has described the ontogeny of both thyroid hormone receptors and the deiodinase sub-types within the placenta and within neurons in human fetal brain.
More recently, there has been interest in the expression of specific thyroid hormone transporters within neurons and glial cells that appear to be expressed in human fetal neuronal cells and play an integral role in the action of Free T3 on fetal neurons.
This overview lecture will describe these homeostatic mechanisms within animal and human pregnancy.
06 - 07 Nov 2006
Society for Endocrinology