Aim. To analyze an incidence rate of polymorphisms and combinations of genes AGT-704T> C, AGT-521C> T, AGTR1-1166A> C, AGTR2-1675G> A, еNO3-786T> C, еNOS3-894G> C, ADD1-1378G> T, CYP11B2 -304C> T, GNB3-825C> T and to assess their association with a risk of severe pre-eclampsia. Materials and methods. The study included women of early fertile age (20-35 years old) with spontaneous singleton pregnancy, no bad habits (smoking, alcohol or drug use), no extragenital diseases and no family (mother or sister) or an individual history of pre-eclampsia and with body mass index in the first trimester of pregnancy less than 35 kg/m2. The study group consisted of 100 patients with severe preeclampsia and the control group included 100 women with uncomplicated pregnancy. Genotyping was carried out by method of polymerase chain reaction. Data analysis included compliance with the Hardy - Weinberg law, Cramer's V criterion, χ2 test, odds ratio (OR) and its 95% confidence interval (CI). To assess a distribution of stated polymorphisms of genes and their alleles a general (χ2 test, df=2) and multiplicative (χ2 test, df=1) inheritance models were used. Results and discussion. Patients with severe pre-eclampsia had statistically significantly higher incidence rate of mutant homozygous genotypes AGTR1-1166CC (χ2=5,54; p=0,05) and еNO3-786CC (χ2=23,05; p=1,0E-5). A significant association between a carrier of the mutant homozygous genotype eNO3-786СC (χ2=19,780; p=0,000) and severe pre-eclampsia (OR 45,07, 95% CI 2,68-759,30) was found out. Combinations of mutant alleles of potentially predictive polymorphisms of vasoactive genes in women with preeclampsia were recorded 7,7 times more often (23% vs 3%; χ2=17,683, p=0,000; average Cramer's V link) which led to a significant association link with a risk of a disease complication (OR 9,658, 95% CI 2,795-33,367). Conclusion. A synergistic interaction between polymorphic loci in severe preeclampsia was established. The mutant homozygous genotype eNO3-786СC as well as a combination of at least two mutant alleles of genes - candidates for arterial hypertension or their combination with the mutant gene ADD1-1378TT or GNB3-825TT can claim a role of molecular and genetic predictors of severe preeclampsia.

Диагностика идиопатической нормотензивной гидроцефалии (иНТГ) вызывает затруднения из-за схожей симптоматики с нейродегенеративными заболеваниями. Не всегда данные магнитно-резонансной томографии (МРТ) головного мозга и инвазивные методы (тап-тест, наружный люмбальный дренаж, инфузионный тест) позволяют точно установить диагноз иНТГ, тем более когда у пациентов имеется сопутствующая патология. В связи с этим возрастает роль биомаркеров цереброспинальной жидкости (ЦСЖ) в дифференциальной диагностике иНТГ и коморбидных заболеваний на ранних стадиях. Цель исследования-анализ данных литературы о современных представлениях о биомаркерах в ликворе и их роли в дифференциальной диагностике иНТГ с нейродегенеративными заболеваниями головного мозга.

The paper provides data on current neuroimaging techniques for diagnosing Alzheimer’s disease and vascular cognitive impairment (CN). Structural neuroimaging methods can identify potentially treatable diseases leading to dementia and assess the magnitude and localization of atrophic and cerebrovascular changes in brain tissue. Particular attention is paid to the specific signs of Alzheimer’s disease: to the visual assessment of sections and the use of various rating scales (GCA, MTA, Koedam). Vascular changes that are most significant for the development of CI are considered. A new approach to diagnosing CI is presented, by taking into account the biomarkers of amyloidosis, tauopathy, neurodegeneration, and cerebrovascular damage. The results of the authors’ own investigations using positron emission tomography, single photon emission computed tomography, magnetic resonance spectroscopy, and functional magnetic resonance imaging at rest allow these techniques to be recommended for the early diagnosis of CI of different genesis.

Alzheimer’s disease is the most common cause of dementia among the elderly. Te pathological changes characterize by the deposition of amyloid plaques and the formation of neurofybrillar tangles in the brain. Te most signifcant role in the pathogenesis of neurodegeneration development is deposition of β-amyloid, vascular risk factors, the presence of a genetic predisposition, and the dysregulation of the bloodbrain barrier. Recent studies have demonstrated the role of the glymphatic system in the clearance of betaamyloid through the perivascular spaces of Virchow-Robin.

Cognitive impairment is a global medical and social problem. Alzheimer’s disease (AD) is the most common disease leading to the development of cognitive impairment and dementia. Arterial hypertension (HTN) is considered to be the strongest risk factor for the development of both vascular dementia and AD. Recent studies have demonstrated the importance of the glymphatic system in removing β-amyloid from the brain through the perivascular Virchow–Robin spaces. The interest is that the adequate functioning of the glymphatic system mainly depends on the level of blood pressure during the day and the quality of sleep. In this article, we will consider the main mechanisms of the HTN influence on the glymphatic system, brain substance-related damage and the development of cognitive impairment.