Advances in Gerontology最新文献

Abstract

The main pathophysiological triggers of obstructive sleep apnea (OSA) syndrome are oxidative stress and hypoxia. These factors cause cellular and molecular disorders that characterize the aging process. The fact that the blood content of the differentiating protein GDF-15 (the “protein of senility”) increases with age, which was revealed by a number of researchers, arouses interest in its assessment in patients with OSA. Thus, the purpose of this study is to evaluate changes in the content of GDF-15 under conditions of oxidative stress and intermittent nocturnal hypoxia with normalization of the nocturnal oxygen gradient in patients with OSA. The study involves 30 men aged 45–55 years with moderate OSA (main group, MG1) and 35 men of the same age without OSA (control group, CG). The MG1 patients are prescribed aРАР therapy (automatic positive airway pressure) during sleep for 6 months. These patients after treatment make up the second main group, MG2. Blood is taken from all the subjects in the morning to determine the content of lipid-peroxidation products and components of antioxidant defense (LPO-AOD) and GDF-15. The following methods are used to evaluate the results: questionnaires, polysomnographic monitoring, spectrometric and radioimmunoassay methods, and statistical analysis. According to the results, an imbalance of the LPO-AOD system with the predominance of oxidation processes in MG1 is revealed demonstrating the coefficient of oxidative stress, which statistically significantly decreases with the elimination of hypoxia and improvement of sleep structure. GDF-15 demonstrates significant differences between MG1 and CG patients with a predominance of content in the group of MG1 patients with OSA. In comparison with the indicators of MG2, no statistical differences are revealed.

Abstract

Stroke is a leading cause of disability worldwide, significantly affecting not only the health and quality of life of survivors but also of those who provide daily care to these individuals, requiring reliable measurement tools to assess these impacts. The Adult Carer Quality of Life Questionnaire (AC-QoL) is a recent and valid instrument, surpassing the limitations of previous tools. Given the lack of validated measures to assess the quality of life (QoL) of carers of stroke survivors, this study aimed to explore the psychometric properties of the AC-QoL among Portuguese informal carers of stroke survivors. After a linguistic adaptation to Portuguese of the AC-QoL, informal carers (n = 443) of stroke survivors hospitalized in all Stroke Units of the North of Portugal (n = 12), were invited to complete the AC-QoL and a structured questionnaire assessing their sociodemographic, caregiving-related, and psychological features, 18 to 24 months post-stroke (November 2019 and August 2021). Psychometric properties were investigated through confirmatory factor analyses and reliability evaluation. Linear regression models assessed convergent-discriminant validity with carers’ sociodemographic, caregiving-related, and psychological characteristics. Our results found a replicable eight-factor structure from the original AC-QoL, revealing good adequacy (CFI = 0.899] and high internal consistency (alpha = 0.904]. Convergent-discriminant validity was satisfactory with burden, anxiety, and depression being inversely associated with the overall score of the AC-QoL. Being younger, married, with higher education, being the son/daughter, and living with the stroke survivor were associated with higher scores of QoL. The Portuguese version of the AC-QoL is a comprehensive, simple, reliable and valid instrument to assess informal stroke carers’ QoL. The AC-QoL can be a valuable tool contributing to devise strategies promoting the well-being and social integration of stroke survivors and their informal carers.

Zinc deficiency in the human body occurs when there is a lack of this trace element in food and water, which is especially important for the territories of the North that belong to biogeochemical provinces. The surface waters of the Republic of Karelia are ultra fresh and low mineralized. In this work, the zinc content in the hair of the older age group of residents of the Republic of Karelia (Petrozavodsk) is determined and the prevalence of this deficiency is assessed. To conduct the study, the method of atomic emission spectrometry and mass spectrometry with inductively coupled argon plasma are used. To assess the severity of hypozincosis, we use a point scale corresponding to the degree of deviation of the zinc content from the reference values. Hypozincosis is typical for 74.5% of the subjects, and a zinc deficiency was significantly more typical for people over 60 years of age than for young people aged 20–25 years. It is shown that the first degree of deviation of the level of zinc in hair in the direction of either a decrease or an excess of the concentration of the element compared to the reference values is the most common, which is regarded as a “predisease” state. Moreover, in the age group of 20–25 years, an excess of zinc is significantly more often diagnosed, and in people over 60 years old, a deficiency of this element is diagnosed. No gender differences are found in zinc deficiency. It is assumed that the natural, ecological, and social living conditions of this region are the cause of the development of hypozincosis. It is likely that people of older age groups living in the territories of the European North require the additional intake of mineral complexes. The composition of such multimineral complexes must necessarily include zinc, and in greater quantities than is recommended for residents of central Russia.

In people over 60 years, the most common diseases are those of the cardiovascular system and geriatric syndromes. Dyslipidemia and hyperglycemia are traditional cardiovascular risk factors. However, their impact on the development of major geriatric syndromes among people over 60 years remains unclear. The relationship between the presence of type-2 diabetes mellitus and the development of frailty, sarcopenia, and cognitive impairment depends on age. The influence of chronic hyperglycemia on geriatric syndromes decreases with increasing age and acquires a neutral role in long-living people. Recent studies have shown that low high-density lipoprotein (HDL) levels in people over 60 years old are associated with the development of frailty, sarcopenia, and cognitive impairment.

We have studied the concentration of vitamins A (retinol) and E (α-tocopherol) in the tissues of the bank vole (Myodes (Clethrionomys) glareolus) and common shrew (Sorex araneus) inhabiting the northern periphery of its natural habitat. The distribution of vitamin A in the common shrew and bank vole tissues is similar: the highest concentration is found in the liver, and the lowest level is found in the heart. Age-related differences in the retinol concentration are detected in the kidneys of the two species, as well as in the skeletal muscle of the shrew. A significantly lower vitamin E concentration is found in all organs of young shrews before wintering, compared to adult overwintered animals, while in the bank vole no such age-related differences are found. Interspecies differences in the levels of vitamins A and E in the liver of overwintered animals are revealed. The results obtained show that the concentration of vitamins A and E in the tissues of the bank vole and the common shrew is determined by metabolic processes and the ecological characteristics of the species. The level of vitamins in the common shrew depends largely on age.

Parkinson’s disease (PD) is a neurodegenerative disease, the main predisposing factor of which is aging. Today, the majority of people suffering from PD are over 65 years of age. This disease leads to motor and nonmotor deficits, significantly reducing the quality and length of life. One of the symptoms of nonmotor manifestations is a decrease in cognitive function, including impaired memory and learning ability. Fear is a response to a threatening situation that is always real and well defined. Fear memory is a form of memory that remains stable throughout the life of an organism. Using neurotoxic and genetic models of laboratory animals, it is possible to reproduce the symptoms of the disease to decipher the pathological features, genetic factors, and mechanisms underlying PD. In addition, disease modeling makes it possible to study the mechanisms of fear memory for a given disease with assessment of the response of fear conditioning to a given context or sound/light as the conditioned signal (contextual and signal response to fear conditioning), and the conditioned response of passive avoidance. The cognitive and motor symptoms of PD refer to different brain regions. The structures that play a critical role in fear-memory mechanisms are the hippocampus and the amygdala. The hippocampus is responsible for “creating context” and the amygdala is responsible for “creating fear,” and as a result of the convergence of signals, a fear-memory trace is formed. Using mice and rat models of PD, experimental evidence has been obtained for the significant contribution of the hippocampus and amygdala to the mechanisms of fear-memory impairment. In addition, deficits in fear memory in Parkinson-like conditions correlate with α-syn neuropathology (alpha-synuclein deposits) in the hippocampus and amygdala. Dysfunction of the nigrostriatal system through the mechanisms of neuroinflammation and oxidative stress also causes the impairment of fear memory. Thus, the mechanism of fear-memory deficit in PD may be a change in information processing in the hippocampus/prefrontal cortex/amygdala networks due to identified impairment in synaptic plasticity, the development of neuroinflammation, oxidative stress, and α-syn-neuropathology.

Studying the mechanisms of age-related changes in vascular reactions and applying the acquired knowledge in clinics can help reduce complications and mortality from diseases of the cardiovascular system, the frequency of which increases with age. This study is important because with aging, endothelial dysfunction increases and cerebral circulation disorders caused by the occurrence of ischemic foci are observed. One of the main elements in the regulation of vascular tone, along with many important mechanisms, is potassium ion channels. In this work, we study age-related changes in the role of calcium-activated potassium channels (BK_Ca) in the acetylcholine-mediated dilation of cerebral arteries in Wistar rats, since their contribution to vasodilation in aging is poorly understood. Using intravital microphotography (×470), we compare the responses of pial arteries to acetylcholine chloride (ACh, 10^–7 M, 5 min) in the absence and against the background of BK_Ca blockade with tetraethylammonium chloride (TEA, 2 mM, 5 min) in Wistar rats 4, 6, 9, 18 and 24 months old. Changes in the contribution of BK_Ca to vascular dilation are assessed by changes in the number of dilations of the pial arteries upon exposure to ACh after BK_Ca blockade, measuring the width of vessels in 3 separate groups of arteries: small (with a diameter of less than 20 μm), medium (20–40 μm), and large (more than 40 μm). It has been shown that ACh-induced dilation depends on the initial diameter of the arteries. The inhibition of BK_Ca activity in 4-month-old rats reduces the number of ACh-induced dilations in all groups of arteries studied. Compared to 4-month-old rats, in 6- and 18-month-old rats the contribution of BK_Ca channels to the dilation of small arteries is reduced, in 9- and 24-month-old rats the contribution of BK_Ca channels to the dilation of medium arteries is increased; the contribution of BK_Ca to the dilation of large arteries decreases starting from 6 months of age. Dilation of the pial arteries of Wistar rats at the age of 4–24 months depends on the initial diameter of the vessel. BK_Ca play a significant role in the ACh-mediated dilation of these vessels. Age-related impairments in the contribution of these channels to the ACh-mediated dilation of pial arteries develop gradually, have a wave-like course and depend on the diameter of the arteries. The identified disturbances in the functional activity of BK_Ca can serve as therapeutic targets for the creation of new technologies for the treatment of age-related lesions of cerebral vessels.

In modern conditions of constant adverse effects on living organisms, such as environmental pollution or global climate change, the study of deeply conserved mechanisms that contribute to the adaptation of animals to such conditions is of particular relevance. The influence of stress suffered at early stages of development on the formation of fitness and the endocrine status of adults has been repeatedly shown in various species of mammals. However, similar studies on arthropods have not previously been carried out, and one of the key differences between the ontogeny of holometabolous insects from mammals is metamorphosis, including the formation of a pupa and the histolysis of tissues and organs with the subsequent formation of new structures from its products and imaginal discs, which are formed in early ontogenesis. As a result, an almost new organism, an imago, is formed. Are the metabolic changes that occurred in the insect’s body under the influence of unfavorable external influences before the imaginal moult preserved, or does metamorphosis “erase” them? To answer this question, the effect of heat stress experienced by the larvae of Drosophila melanogaster on such signs of adult fitness as longevity, response to acute heat stress, and resistance to it is studied. The study results show that early mortality is reduced due to larval stress in both D. melanogaster males and females, although no changes in the maximum lifespan are recorded. At the same time, early stress leads to a decrease in resistance to acute heat stress and a corresponding drop in alkaline-phosphatase activity in both sexes. Thus, we can conclude that heat stress experienced by D. melanogaster during the larval stage is not “reset” by metamorphosis, and causes significant changes in the fitness of adult individuals.

Transcription regulation is required for correct differential gene expression, which determines the development and function of all cells in the organism throughout the lifespan, ensuring adaptability to continuously changing environments. Altered transcriptional regulation causes gene function rearrangements, which alter the phenotype, including aging rate and lifespan. In this regard, there has recently been a great interest in the application of technologies based on the “rejuvenation” of the transcriptome due to the modification of regulatory mechanisms that determine the level and pattern of gene expression. To develop such an approach to slowing down aging and prolonging life, it is important to understand how the transcription of individual genes and the entire transcriptome changes with age, as well as how the transcriptional machinery of the cell and mechanisms of transcription regulation are related to the aging process and longevity control. Addressing these issues in the review, we discuss the prospects of using transcription regulation as a strategy for extending life and improving its quality.