Potential Possibilities of Nuclear Medicine Methods in Diagnostics Age Changes of the Cardiovascular System.

2021 ◽  
Vol 66 (5) ◽  
pp. 59-65
Author(s):  
M. Vorontsova ◽  
A. Obrezan ◽  
A. Obrezan

In connection with the increase in the average age of the world's population, the problem of preventing premature aging and the treatment of age-related diseases is coming to the fore. The main direction in the implementation of this goal is to influence the key molecular mechanisms of aging in order to suppress pathological processes and activate the defense systems of the cell and the body as a whole. In order to solve this daunting task, it is necessary to have in the arsenal not only various means of intervention in the aging process, but also diagnostic methods that would allow to fully verify these processes and evaluate the effectiveness of medical interventions.

2020 ◽  
Vol 22 (3) ◽  
pp. 4-18
Author(s):  
Olga O. Golounina ◽  
Valentin V. Fadeev ◽  
Zhanna E. Belaya

Aging is a multi-factor biological process that inevitably affects everyone. Degenerative processes, starting at the cellular and molecular levels, gradually influence the change in the functional capabilities of all organs and systems. Progeroid syndromes (from Greek. progērōs prematurely old), or premature aging syndromes, represent clinically and genetically heterogeneous group of rare hereditary diseases characterized by accelerated aging of the body. Progeria and segmental progeroid syndromes include more than a dozen diseases, but the most clear signs of premature aging are evident in Hutchinson-Guilford Progeria Syndrome and Werner Syndrome. This review summarizes the latest scientific data reflecting the etiology and clinical picture of progeria and segmental progeroid syndromes in humans. Molecular mechanisms of aging are considered, using the example of progeroid syndromes. Modern possibilities and potential ways of influencing the mechanisms of the development of age-related changes are discussed. Further study of genetic causes, as well as the development of treatment for progeria and segmental progeroid syndromes, may be a promising direction for correcting age-related changes and increasing life expectancy.


2007 ◽  
Vol 32 (5) ◽  
pp. 954-966 ◽  
Author(s):  
Christy S. Carter ◽  
Tim Hofer ◽  
Arnold Y. Seo ◽  
Christian Leeuwenburgh

The aging process results in a gradual and progressive structural deterioration of biomolecular and cellular compartments and is associated with many pathological conditions, including cardiovascular disease, stroke, Alzheimer’s disease, osteoporosis, sarcopenia, and liver dysfunction. Concomitantly, each of these conditions is associated with progressive functional decline, loss of independence, and ultimately disability. Because disabled individuals require care in outpatient or home care settings, and in light of the social, emotional, and fiscal burden associated with caring for an ever-increasing elderly population, research in geriatric medicine has recently focused on the biological mechanisms that are involved in the progression towards functional decline and disability to better design treatment and intervention strategies. Although not completely understood, the mechanisms underlying the aging process may partly involve inflammatory processes, oxidative damage, mitochondrial dysfunction, and apoptotic tissue degeneration. These hypotheses are based on epidemiological evidence and data from animal models of aging, as well as interventional studies. Findings from these studies have identified possible strategies to decrease the incidence of age-related diseases and delay the aging process. For example, lifelong exercise is known to extend mean life-span, whereas calorie restriction (CR) increases both mean and maximum life-span in a variety of species. Optimal application of these intervention strategies in the elderly may positively affect health-related outcomes and possibly longevity. Therefore, the scope of this article is to (i) provide an interpretation of various theories of aging from a “health-span” perspective; (ii) describe interventional testing in animals (CR and exercise); and (iii) provide a translational interpretation of these data.


2020 ◽  
Vol 50 (6) ◽  
pp. 1504-1512
Author(s):  
Güler ÖZTÜRK ◽  
Kazime Gonca AKBULUT ◽  
Şevin GÜNEY

The aim of this review is to summarize current studies on the relationship between melatonin and aging. Nowadays, age-related diseases come into prominence, and identifying age-related changes and developing proper therapeutic approaches are counted as some of the major issues regarding community health. Melatonin is the main hormone of the pineal gland. Melatonin is known to influence many biological processes in the body, including circadian rhythms, the immune system, and neuroendocrine and cardiovascular functions.Melatoninrhythms also reflect the biological process of aging. Aging is an extremely complex and multifactorial process. Melatonin levels decline considerably with aging and its decline is associated with several age-related diseases. Aging is closely associated with oxidative damage and mitochondrial dysfunction. Free radical reactions initiated by the mitochondria constitute the inherent aging process. Melatonin plays a pivotal role in preventing age-related oxidative stress. Coronavirus disease 2019 (COVID-19) fatality rates increase with chronic diseases and age, where melatonin levels decrease. For this reason, melatonin supplementation in elderly could be beneficial in COVID-19 treatment. Therefore, studies on the usage of melatonin in COVID-19 treatment are needed.


Author(s):  
A. O. Radchenko ◽  
T. M. Bondar ◽  
A. V. Potapenko

Aging is characterized with a gradual aggravation of organ function throughout life and can occur both physiologically and prematurely. With premature aging there is an early decrease in the adaptive mechanisms of all physiological systems of the body, there is a significant reduction in physical and mental activities, that contributes to the early development of age−related pathology. Genetic and epigenetic factors, as well as environmental ones can be the causes of different rates of aging. It is not possible to accurately determine the onset of old age by biological characteristics, because people with the same calendar age are not always the same as for biological one. To establish the association of age−related disease factors with the markers of premature aging and biological age in the patients of various age groups, a study was performed in the patients aged 25−44 and 45−59 years with moderate cardiovascular risk in accordance with the SCORE scale. The primary task for predicting and preventing the age−associated diseases is to identify genetic, molecular and cellular factors that determine the rate of aging and increase the risk of age−associated diseases. The role of cardiovascular risk factors in premature aging has been determined. It is established that the most important factors that lead to an increase in biological age and formation of age−associated diseases are the disorders of lipid and carbohydrate metabolism and level of oxidative stress, importance of which progresses with age. The relationship between cardiovascular risk factors and biological age, estimated with different methods, their influence on telomere length, that allows the designing of an algorithm to determine the markers of premature aging in different age groups for early and effective prevention of metabolic−associated diseases, has been established. Key words: biological age, cardiovascular risk, premature aging, telomere length.


2020 ◽  
Vol 2020 ◽  
pp. 1-14
Author(s):  
Yulia K. Denisenko ◽  
Oxana Yu Kytikova ◽  
Tatyana P. Novgorodtseva ◽  
Marina V. Antonyuk ◽  
Tatyana A. Gvozdenko ◽  
...  

Metabolic syndrome (MetS) has a worldwide tendency to increase and depends on many components, which explains the complexity of diagnosis, approaches to the prevention, and treatment of this pathology. Insulin resistance (IR) is the crucial cause of the MetS pathogenesis, which develops against the background of abdominal obesity. In light of recent evidence, it has been shown that lipids, especially fatty acids (FAs), are important signaling molecules that regulate the signaling pathways of insulin and inflammatory mediators. On the one hand, the lack of n-3 polyunsaturated fatty acids (PUFAs) in the body leads to impaired molecular mechanisms of glucose transport, the formation of unresolved inflammation. On the other hand, excessive formation of free fatty acids (FFAs) underlies the development of oxidative stress and mitochondrial dysfunction in MetS. Understanding the molecular mechanisms of the participation of FAs and their metabolites in the pathogenesis of MetS will contribute to the development of new diagnostic methods and targeted therapy for this disease. The purpose of this review is to highlight recent advances in the study of the effect of fatty acids as modulators of insulin response and inflammatory process in the pathogenesis and treatment for MetS.


2019 ◽  
Vol 24 (44) ◽  
pp. 5245-5251 ◽  
Author(s):  
David Schröter ◽  
Annika Höhn

Aging is one of the biggest risk factors for the major prevalent diseases such as cardiovascular diseases, neurodegeneration and cancer, but due to the complex and multifactorial nature of the aging process, the molecular mechanisms underlying age-related diseases are not yet fully understood. Research has been intensive in the last years aiming to characterize the pathophysiology of aging and develop therapies to fight age-related diseases. In this context advanced glycation end products (AGEs) have received attention. AGEs, when accumulated in tissues, significantly increase the level of inflammation in the body which has long been associated with the development of cancer. Here we discuss the classical settings promoting AGE formation, as well as reduction strategies, occurrence and relevance of AGEs in cancer tissues and the role of AGE-interaction with the receptor for advanced glycation end products (RAGE) in cancer initiation and progression.


2021 ◽  
Vol 20 (6) ◽  
pp. 96-102
Author(s):  
Ilmira R. Gilmutdinova ◽  
Irina S. Kudryashova ◽  
Elena Yu. Kostromina ◽  
Maksim Yu. Yakovlev ◽  
Inessa Kh. Yafarova ◽  
...  

From the biomedicine point of, view ageing is a natural process, characterized by a gradual decrease in the physiological integrity and adaptive abilities of the body, leading to a violation of its functions and an increase in the risk of death with age. Demographic aging of the population is a serious socio-economic problem, both in Russia and around the world. The main cellular and molecular signs of aging include genome instability, telomere shortening, epigenetic alterations, impaired proteostasis, impaired nutrient recognition, mitochondrial dysfunction, cellular aging, the stem cell pool depletion and changes in intercellular interaction, extracellular matrix rigidity, as well as activation of retrotransposons and chronic inflammation. For these reasons, in modern healthcare, preventing premature aging and treating age-related diseases is becoming a priority task. This review presents modern approaches to the quantitative assessment of the aging process using aging biomarkers as functional parameters reflecting the biological organism age at the molecular, cellular, and organismal levels. This work also considers the actual non-drug and drug interventions allowing to slow down the development of age-associated pathological processes, allowing you to increase the quality and duration of life.


2019 ◽  
pp. 14-25
Author(s):  
Vladimir N. Anisimov

The review summarizes the modern knowledge of the impact of day-night, light-darkness rhythm disorders on the aging process and on the risk of development of the age-related conditions. Significant evidence has been obtained of that the constant artificial illumination and the daylight of the North has a stimulating effect on the occurrence and de-velopment of tumours in laboratory animals. It has been shown that long-term shift work, trans-meridian flights (jet-lag) and insomnia increase the risk of cardiovascular diseases, diabetes mellitus, and ma-lignancies in humans. Particular attention is given to the studies where the relationship between light intensity, light wavelength and its ability to suppress the synthesis of melatonin produced at night in the pineal gland, are investigated. It has been established that melatonin synthesis is most effectively suppressed with blue light sources of a wave-length from 446 to 477 nm. The use of exogenous melatonin prevents premature aging of the reproductive system and the body as a whole prevents the development of immunesuppression, metabolic syndrome and tumours caused by light pollution. An urgent task is to develop recommendations for optimizing the illumination of workplaces and res-idential premises, of cities and towns as a preven-tion measure for premature aging and age-related pathology, which, ultimately, will contribute to the long-term maintaining of performance and improv-ing the quality of life.


2018 ◽  
Vol 2018 ◽  
pp. 1-6 ◽  
Author(s):  
Makoto Kuro-o

The basic research of aging has been primarily focused on elucidating mechanisms of aging and longevity that are evolutionarily conserved from yeasts to primates. Such efforts have culminated in the notion that (1) senescence at the cellular level is associated with aging at the organismal level and that (2) calorie restriction and growth suppression decelerate aging. However, these important findings in the basic research have not necessarily been linked to improvement of daily medical practice in the aging society. It has become increasingly important to investigate mechanisms of aging unique to mammals or humans and apply the research fruits for the treatment of major age-related disorders to extend the health span. Seminal studies on the klotho mouse, a mutant exhibiting a premature aging syndrome, have identified phosphate as a proaging factor in mammals. In this review, mechanisms of phosphate-induced premature aging and potential therapeutic targets will be discussed, which may be directly applicable for developing novel strategies for the treatment of chronic kidney disease and its complications.


2019 ◽  
Vol 3 (Supplement_1) ◽  
pp. S101-S101
Author(s):  
Ning Zhang ◽  
Susan Weintraub ◽  
Nicolas Musi

Abstract Skeletal muscle is one of the most abundant tissues in the body. In addition to its key roles in body support, movement and metabolic homeostasis, muscle also functions as an endocrine/secretory organ producing and releasing proteins into the circulation that modulate distant tissues (i.e. myokines). Considering that muscle mass and function changes with advancing age, here we tested the hypothesis that aging alters the muscle secretome profile. After euthanasia, soleus muscles from sedentary young and old mice were dissected, and incubated in oxygenated KRB buffer for 2 h. The buffer was subjected to in-gel trypsin-digestion and peptides analyzed by mass spectrometry. The concentration of 36 proteins were significantly (P<0.05) elevated in the young vs. the old group. In contrast, only 7 proteins were significantly elevated in the old group. Some notable differences include those in HSPA1B and HSPA5 that were detected only in the young group. HSPA8 also was significantly elevated by 1.8-fold (P<0.05) in the young versus the old group. Another prominent difference between groups involved translationally controlled tumor protein (TCTP), a critical regulator of apoptosis/carcinogenesis, that was elevated by 7-fold in the young vs. the old group (P<0.05). These results indicate that aging alters the muscle secretion profile. Identified differences in the muscle secretome could reflect intrinsic changes in muscle cells with age. Because these myokines are released into the circulation, it is also possible that myokine secretion is a regulated cellular process by which muscle communicates and modulates the aging process in distant tissues.


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