thyroid, brain, development, pollutants, diabetes

What is it about?

hypothyroidism disrupts the developmental thyroid-brain axis

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Why is it important?

Thyroid hormone deficiency during a critical developmental period can impair cellular migration and development of neuronal networks. Neuronal outgrowth and cellular migration are dependent on normal microtubule synthesis and assembly and these latter processes are regulated by thyroid hormones (Nunez et al., 1991). During cerebral development, postmitotic neurons forming near the ventricular surface must migrate long distances to reach their final destination in the cortical plate where they form a highly organized 6-layer cortical structure (Porterfield, 2000). Appropriate timing of this migration is essential if normal connectivity is to be established. This migration depends not only upon specialized cells such as the radial glial cells that form a scaffolding system but also on specific adhesion molecules in the extracellular matrix that are associated with the focal contacts linking migrating neurons with radial glial fibers (Mione and Parnavelas, 1994). These neurons migrate along radial glial fibers, and following neuronal migration, the radial glial cells often degenerate or become astrocytes (Rakic, 1990). Migration also depends on adhesive interactions involving extracellular matrix proteins such as laminin and the cellsurface receptor integrin (Porterfield, 2000). Disorders of neuronal migration are considered to be major causes of both gross and subtle brain abnormalities (Rakic, 1990). Hypothyroidism during fetal and neonatal development results in delayed neuronal differentiation and decreased neuronal connectivity (Nunez et al., 1991).

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