Pathology

Biography

Biography: Mehmet Eray Alcigir

Abstract

Thyroid hormones (THs) has an important role in morphogenesis and neuronal development for mammalian and nonmammalian brain. In infants, partial or complate loss of thyroid function causes congenital hypothyroidism characterized by retarded neuronal migration, neuropil deficit, Purkinje cells destruction can be also seen in congenital hypothyroidism. Apoptosis (programmed cell death) is a well known mechanism that cause pathomorphlogical changes in central nervous system in congenital hypothyroidism. The activation of caspase proteases, especially caspase-3 and caspase-9, mainly leads to fragmentation of DNA in nuclei and other cellular structures and is essential for apoptosis . Although the roles of caspase-3 and caspase-9 in neurologic changes caused by congenital hypothyroidism are not fully understood, it was reported that they take in place in the process of different neurologic events. In the study, caspase-3 and caspase-9 expressions and DNA in situ fragmentation activities were evaluated in central nervous system of developing rat with congenital hypothyroidism. H&E and Kluver-Barrera staining showed neuronal degeneration and demyelination. Neuronal degenerations in front and mid brain were densed. Demyelination were more widespread in 10 day old rat pups. Caspase-3 and -9 positivities were strickly found in layers of cerebral cortex and hypocampus and stratum granulare and gangliosum cells of cerebellum in all pups. Oligodenroglia and astroglia were remakably positive in 30 day old pups. Caspase-9 positivities were attended in also neurons of thalamus, medulla oblangata. TUNEL positivities in 30 day old pups were as commonly as that of caspases. The results showed neuronal degeneration were more extent in cerebrum during one thirh of postnatal period. Substantia grisea and alba of cerebrum-cerebellum and also m.oblangata and pons were widely effected in first month of life.