Abstract:
Thyroid hormones are fundamental to the development of the brain and ensure its functioning throughout life. Hyperhomocysteinemia (HHCy) has been shown to be an important risk factor for cerebrovascular
disease leading to stroke, Alzheimer’s disease, and vascular dementia. Recent experimental studies have shown the effect of HHCy on cerebrovascular biology and the molecular mechanisms that explain these changes.The aim – to define the submicroscopic changes in the sensorimotor area of the cerebral cortex under influence of HHCy against the background of hyper- and hypothyroidism. Object and methods. HHCy was modeled by administering exogenous HCy to animals in the form of thiolactone at a dose of 100 mg/kg of body weight once a day for 28 days. Hyperthyroidism (intragastric L-thyroxine for 21 days 200 µg/kg*day), hypothyroidism (thiamazole 10 kg*day) for 21 days. Separate groups of animals were injected with L-thyroxine and thiamazole in parallel with HCy. Study results. HHCy was accompanied by destructively changed organelles, submicroscopic changes in astrocytic glia and blood capillaries. In turn, hyperthyroidism caused hypertrophy of mitochondria, a decrease in the number of ribosomes and destructive changes in hemocapillaries. The most significant alterative and degenerative changes in neurocytes of the cortex of the large hemispheres under conditions of hyperthyroidism and HHCy. Submicroscopically, the most profound violations of their ultrastructure were found in the neurons of animals that were modeled with HHCy and hypothyroidism compared to all previous experimental groups. Conclusions. Submicroscopic studies of the sensorimotor area of the cortex of the cerebral hemispheres of the experimental groups under conditions of simulated HHCy, hypo- and hyperthyroidism, and especially under conditions of their combined influence, established deep submicroscopic neurodegenerative changes in the cerebral cortex. Established neurodegenerative changes in cortical neurocytes occur against the background of neurovascular disorders and alteration of neuroglia.
