Iodine and Brain Disorders
What is it about?
Thyroid Hormones (THs) play an essential role in development and hormone deficiency during critical phases in fetal life may lead to severe and permanent brain damage. Maternal iodine deficiency is considered the most common cause of fetal TH deficiency, but the problem may also arise in the fetus/neonates. Due to defects in fetal thyroid gland development or hormone synthesis, clinical symptoms at birth are often mild as a result of compensatory maternal TH supply. A shortage of THs starting at the early stages of pregnancy results in neurological deficits that cannot be rescued by exogenous TH addition at later stages. Neonates are more sensitive than adults to the effects of iodine deficiency. Thus, these disturbances may lead to abnormalities in the neuronal network and may result in mental retardation and other neurological defects, including impaired motor skills and visual processing. Thus, iodine defenses programmes can avoid adverse neurodevelopmental consequences in mothers and their offspring.
Why is it important?
Defects in synaptic architecture induced by TH insufficiencies, as well as deficiencies in protein substrates involved in complex signaling pathways serious for synaptic plasticity, culminate to disturb hippocampal neurophysiological function. An irregular laminar distribution has been described in the auditory cortex of hypothyroid rats, including an increased number of neurons in layers V/VI, a concomitant diminution in layers II to IV, and the abnormal presence of neurons in the subcortical white matter. Finally, a reduction, or absence, of TH during brain maturation yields molecular, morphological and functional alterations in hippocampus. Interestingly, the neurodevelopmental impairments induced by hypothyroxinemia suggest an independent role of T4.
The following have contributed to this page: Ahmed R. G.