Молодежный инновационный вестникМолодежный инновационный вестник2415-7805Федеральное государственное бюджетное образовательное учреждение высшего образования "Воронежский государственный медицинский университет имени Н.Н. Бурденко" Министерства здравоохранения Российской Федерации6512Conference ProceedingsHOMOCYSTEINE IS A FACTOR IN THE DEVELOPMENT OF DEMENTIAMedvedevaMargaritamargarita.ms@inbox.ruhttps://orcid.org/0000-0002-7309-59741405202110S12702732202202123022021Copyright © 2021, Молодежный инновационный вестник2021<p>Homocysteine (Hcis) is a sulfur-containing non-protein amino acid. Hcis is a member of the group of endogenous thiols that provide the redox balance of cells. Endogenous thiols can exhibit both pro-and antioxidant properties, depending on their physiological state. Hcis, formed in the methylation reaction of methionine, has neurotoxic properties. Normally, the level of homocysteine in the blood should not exceed 7 mmol/l. It was noted that when the level of Hcis is more than 11.9 mmol/l, the risk of damage to the white matter of the brain is tripled, and an increase in the level of Hcis more than 14 mmol / l doubles the risk of developing Alzheimer's disease. The causes of hyperhomocysteinemia are defects in the structure of genes encoding the necessary enzymes for the neutralization of homocysteine, smoking, taking certain medications, thyroid diseases and metabolic disorders, as well as, most often present in elderly patients, a deficiency of B vitamins (folic acid, B12, B6). The hippocampus is particularly sensitive to the effects of homocysteine. Molecular damage to the nerve cells of the brain structure responsible for the processes of memory formation is accompanied by various cognitive disorders that are prone to progression. The neurotoxicity of homocysteine is due to several mechanisms: on the one hand, the formation of endothelial dysfunction, leading to hypoperfusion of neurons, on the other hand, a direct effect on the nerve cell in the form of oxidative stress, which results in cellular apoptosis.</p>гомоцистеин, гипергомоцистеинемия, сосудистая деменция, болезнь Альцгеймера, фолиевая кислота, витамин В12, генетический полиморфизм.[1. Son P., Lewis L. Hyperhomocysteinemia. StatPearls. 2020.][2. Poddar R., Surojut Paul. Homocysteine-NMDA receptor mediated activation of extracellular- signal regulated kinase leads to neuronal cell death. 2009; 110(3): 1095-1106.][3. Мирошниченко И.И., Птицына С.Н., Кузнецова Н.Н., Калмыков Ю.М. Гомоцистеин – предиктор патологических изменений в организме человека. Русский медицинский журнал. 2009; 4: 224.][4. Tan B., Venketasubramanian N., Vrooman H., Cheng Ching-Yun, Tien Yin Wong, Kamran Ikram Mohammad, Chen C., Hilal S. Homocysteine and Cerebral Atrophy: The Epidemiology of Dementia in Singapore Study. J Alzheimers Dis. 2018; 62(2): 877-885.][5. Камчатнов П.Р., Дамулин И.В. Когнитивные нарушения при дефиците витамина B12, фолиевой кислоты и гипергомоцистеинемии. Клиницист. 2015; 1:18-23.][6. Бутенко А.В. Гомоцистеин: влияние на биохимические процессы в организме человека. Молодой ученый. 2016; 105 (1): 78-82.][7. Мирошниченко И.И., Калмыков Ю.М., Яковлева О.Б., Птицина С.Н. Гомоцистеин и психическое здоровье. Психиатрия. 2010; 44 (2): 67-71.][8. Ganguly P., Alam S Fatima. Role of homocysteine in the development of cardiovascular disease. Nutrition Journal. 2015; 6.][9. Татарникова О.Г., Орлов М.А., Бобкова Н.В. Бета-амилоид и TAY-белок: структура, взаимодействие и прионоподобные свойства. Успехи биологической химии. 2015; 55: 351-390.][10. Smith A David, Refsum H. Homocysteine, B Vitamins, and Cognitive Impairment. Annu Rev Nutr. 2016; 36: 211-239.]