http://hdl.handle.net/20.500.12701/1696 Aging publishes research papers in all fields of aging research 2024-02-18T00:21:52Z http://hdl.handle.net/20.500.12701/1765 Название: An antioxidant specifically targeting mitochondria delays progression of Alzheimer’s disease-like pathology Авторы: Stefanova, Natalia A.; Muraleva, Natalia A.; Maksimova, Kseniya Yi.; Rudnitskaya, Ekaterina A.; Kiseleva, Elena; Telegina, Darya V.; Kolosova, Nataliya G. Краткий осмотр (реферат): Mitochondrial aberrations are observed in human Alzheimer’s disease (AD) and in medical conditions that increase the risk of this disorder, suggesting that mitochondrial dysfunction may contribute to pathophysiology of AD. Here, using OXYS rats that simulate key characteristics of sporadic AD, we set out to determine the role of mitochondria in the pathophysiology of this disorder. OXYS rats were treated with a mitochondria-targeted antioxidant SkQ1 from age 12 to 18 months, that is, during active progression of AD-like pathology in these animals. Dietary supplementation with SkQ1 caused this compound to accumulate in various brain regions, and it was localized mostly to neuronal mitochondria. Via improvement of structural and functional state of mitochondria, treatment with SkQ1 alleviated the structural neurodegenerative alterations, prevented the neuronal loss and synaptic damage, increased the levels of synaptic proteins, enhanced neurotrophic supply, and decreased amyloid-β1-42 protein levels and tau hyperphosphorylation in the hippocampus of OXYS rats, resulting in improvement of the learning ability and memory. Collectively, these data support that mitochondrial dysfunction may play a key role in the pathophysiology of AD and that therapies with target mitochondria are potent to normalize a wide range of cellular signaling processes and therefore slow the progression of AD. 2016-10-06T00:00:00Z http://hdl.handle.net/20.500.12701/1700 Название: Biological markers and cardiac remodelling following the myocardial infarction Авторы: Gruzdeva, Olga; Dyleva, Yulia; Uchasova, Evgenya; Akbasheva, Olga; Karetnikova, Victoria; Kashtalap, Vasiliy; Shilov, Aleksandr; Polikutina, Olga; Slepynina, Yulia; Barbarash, Olga Краткий осмотр (реферат): Aim: To assess growth stimulating factor ST2 and N-terminal pro b-type natriuretic peptide (NT-proBNP) levels in the sera of myocardial infraction (MI) patients, and their correlation with the adaptive and maladaptive variants of cardiac remodelling. Methods: 87 patients (65 male, 22 females; 67±8.36 years) with ST-elevated MI were included in this study, and 67 patients had an adaptive, physiological, while 20 patients had a maladaptive, pathological variant of myocardium remodelling. Results: On day 1, ST2 and NT-proBNP levels were shown to increase 2.4 and 4.5 folds, respectively, compared with those in the control. ST2 levels in patients with maladaptive remodelling were 1.5-fold higher than those in the adaptive remodelling group. On day 12, a decrease in ST2 levels was observed in both groups. NT-proBNP levels increased 1.8 folds in both groups on day 1, compared with those in the controls. Increased ST2 levels on day 1 after MI were shown to increase the risk of maladaptive remodelling 4.5 folds, while high NT-proBNP levels increased this risk 2.3 times. Conclusions: ST2 level determination allows us to predict the risk of maladaptive remodelling with a higher sensitivity and specificity than using NT-proBNP levels. 2019-06-10T00:00:00Z