Abstract
The purpose of the work was to investigate the relationship between telomere length and cognitive function and to identify predictors of cognitive impairment in patients with cerebral atherosclerosis and DM. Materials and methods. 161 patients with stage I—III cerebral atherosclerosis were included in complex clinical and instrumental research.Patients were divided into 2 groups: I — with scores on the MMSE scale < 26 (moderate cognitive deficit, 26 patients), II — with scores on the MMSE scale ≥ 26 (mild cognitive deficit, 135patients). Both groups were comparable in age, sex ratio and telomerase activity (p < 0.05). All patients underwent conventional clinical, laboratory and instrumental (transthoracic echocardiography, electrocardiography, ultrasound Doppler of head and neck, magnetic resonance imaging of the brain) assessments. The relative length of the telomere was measured using a multiplex quantitative real-time polymerase chain reaction. Results and discussion. The analysis revealed that in patients of group I telomere length was statistically significantly shorter, patients were less educated, they had more pronounced situational anxiety, more pronounced thickening of complex intima-media in both carotid arteries, and on the Montreal Cognitive Assessment (MoCA) scale they had severe cognitive impairment (p < 0.05). Group II patients had longer telomeres, more education, and high personal anxiety.An inverse relationship has been established between cognitive decline and the thickness of the intima-media carotid artery complex and a direct relationship between telomere length and duration of education, regardless of the presence of type 2 DM. Conclusions. For patients with cerebral atherosclerosis of different stages withDM, predictors of cognitive impairment are telomere length, thickness of the common carotid arteries and duration of education (AUC = 0.91; 95% CI 0.82—0.96).
Highlights
The purpose of the work was to investigate the relationship between telomere length
Patients were divided into 2 groups
Both groups were comparable in age
Summary
5’-AATCCGTCGAGCAGAGTT-3’ 5’-GCGCGGCTTACCCTTACCCTTACCCTAACC-3’ 5’-ACACTAAGGTTTGGGTTTGGGTTTG GGTTTGGGTTAGTGT-3’ 5’-TGTTAGGTATCC CTATCCCTATCCCTATCCCTATCCCTAACA-3’ 5’-CGGCGGCGGGCGGCGCGGGCTGGGCGGAA ATGCTGCACAGAATCCTTG-3’. Активність супероксиддисмутази (СОД) (КФ 1.1.15.1) у плазмі крові визначали непрямим спектрофотометричним методом на основі реакції супероксид-залежного окиснення кверцетину в лужному середовищі за наявності тетраметилетилендіаміну. Концентрацію ТБК-активних продуктів (МДА) розраховували за калібрувальною кривою, отриманою з використанням комерційного МДА (Sigma, 63287). Вміст відновленого глутатіону (GSH) у плазмі крові визначали спектрофлуориметричним методом з використанням ортофталевого альдегіду, в результаті реакції якого з GSH утворюються високофлуоресцентні продукти, які руйнуються випромінюванням при 350 нм і мають чітко виражений пік флуоресценції при 420 нм [13]. Які впливають на когнітивні функції, використовували метод побудови логістичних моделей регресії: MMSE < 26 балів (помірний когнітивний дефіцит, n = 26) — випадок (Y = 1), MMSE ≥26 балів (легкий когнітивний дефіцит, n = 161) — не випадок (Y = 0).
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