Senescence Senotherapeutics And Mitochondria

Senescence, Senotherapeutics and Mitochondria, Volume 136 offers updates on this unique topics, with chapters covering Cellular Senescence in Aging: Molecular Basis, Implications and Therapeutic Interventions, Mitochondria-associated Cellular Senescence Mechanisms: Biochemical and Pharmacological Perspectives, Mitochondria in cell senescence: Friend or Foe?, The role of mitochondria and mitophagy in cell senescence, Small molecules targeting mitochondrial dysfunction for potential senotheraputics, Senolytic and senomorphic interventions to defy senescence-associated mitochondrial dysfunction, Mitochondrial targeting peptides and probes, Mitochondria-derived peptides in healthy ageing and therapy of age-related diseases, and much more. Other sections cover Targeting of mitostasis-proteostasis axis by antioxidant polysaccharides in neurodegeneration, Phytotherapeutic targeting of the mitochondria in neurodegenerative disorders, Melatonin as mitochondria-targeted drugs, Coenzyme Q-related compounds to maintain healthy mitochondria during aging, Changing ROS, NAD and AMP: a path to longevity via mitochondrial therapeutics, and more. Updates on how mitochondria are closely related to the survival of senescent cells using either mitochondria-targeted senolytic or redox modulator senomorphic strategies Differentiates itself from other books with its multidisciplinary perspectives and multidimensional clinical approaches Offers a novel perspective on both the basic and clinical sciences for a wide group of well-established academicians, students and researchers in medicinal chemistry, gerontology, geriatrics, oncology, pharmacology, pathology, bioinformatics, sports science and nutritional sciences

This book offers comprehensive information on the new and rapidly evolving science of identifying and targeting senescent cells, and on the exciting prospect of new diagnostic and therapeutic opportunities for stopping, and even reversing, the progression of disease and the deterioration of the human body due to ageing. According to recent United Nations data, by 2050 one in six people worldwide will be older than age 65, with peaks rising to one in four people in Europe and North America. Remarkably, the number of persons aged 80 years or older is expected to triple, from 143 million in 2019 to 426 million in 2050. First documented in the 1960s, the concept of cellular senescence as an underlying cause of ageing has been established in the course of the last decade. Using genetically engineered mouse models, researchers have demonstrated that the selective elimination of senescent cells can block and even reverse a number of age-related dysfunctions and pathologies, promoting both better health and longer life in the elderly. These include cardiovascular diseases; neurological disorders; type 1 and type 2 diabetes; inflammatory diseases; fibrosis; geriatric syndromes; chronic diseases resulting in organ dysfunction; the integrity of the musculoskeletal system; and cancer. Some senolytic agents have already progressed into trials. These include UBX0101 for the treatment of osteoarthritis (now in phase II), a cocktail of dasatinib and quercetin for the management of idiopathic pulmonary fibrosis and chronic kidney disease, and ABT-263 in combination with senescence-inducing chemotherapies for the treatment of advanced solid tumours. In addition, the book discusses pathways to early phase clinical trials and translational approaches in medicine and ageing, highlighting new opportunities as well as current limitations, challenges and alternatives. Given its scope, it will benefit a broad audience of advanced educators, researchers, graduate students and practitioners.

Cancer is clearly an age-related disease. Recent research in both aging and cancer has demonstrated the complex interaction between the two phenomena. This affects a wide spectrum of research and practice, anywhere from basic research to health care organization. Core examples of these close associations are addressed in this book. Starting with basic research, the first chapters cover cancer development, mTOR inhibition, senescent cells altering the tumor microenvironment, and immune senescence affecting cancer vaccine response. Taking into account the multidisciplinarity of geriatric oncology, several chapters focus on geriatric and oncologic aspects in patient assessment, treatment options, nursing and exercise programs. The book is rounded off by a discussion on the impact of the metabolic syndrome illustrating the interactions between comorbidity and cancer and a chapter on frailty.This book provides the reader with insights that will hopefully foster his or her reflection in their own research and practice to further the development of this most exciting field. Given the aging of the population worldwide and the high prevalence of cancer, it is essential reading not only for oncologists and geriatricians but for all health practitioners.

Psychsocial aspects of reproductive aging. Clinical aspects of aging of the female reproductive system. Clinical aspects of aging of the male reproductive system. Effect of aging of the ovaries and female gametes on reproductive caapacity. The aging uterus and fallopian tubes. Aging of the male sex accessory organs. Aging effects on the hypothalamicHypophyseal gonadal control system in the rat. Reproductive senescence in rodents: factors in the decline of fertility and loss of regular estrous cyples. Recent studies on neuroendocrine control of reproductive senescence in rats. An effect of reproductive aging: increased risk of genetically abnormal of spring.

The demographic shift in the average age of the population worldwide calls for careful attention to the nutritional and health needs of the elderly. Frailty has been associated with increased disability, postsurgical complications and increased mortality; in a frail state, older adults are at greater risk for adverse outcomes, including falls and admissions to hospital and nursing homes. Despite the strong associations between frailty and subsequent poor outcomes, limited attention to this common geriatric condition has been paid in clinical settings. Emerging evidence suggests that both behavioral (nutrition and physical activity) and pharmacologic interventions may be effective in the treatment and prevention of the frailty syndrome. The papers in this book address our current understanding of the biological basis, clinical presentation and therapeutic interventions that target frailty. They highlight the transitional nature of research on the frailty syndrome and identified key unmet needs and areas for future investigation in this expanding field.

Sarcopenia: Molecular, Cellular, and Nutritional Aspects describes the progressive loss of skeletal muscle mass and strength, defined by Rosenberg in 1997 as a hallmark of aging and referred to as “sarcopenia.” As life expectancy continues to increase worldwide, sarcopenia has become a major public health issue. The condition worsens in the presence of chronic diseases accelerating its progression. Sarcopenia is not considered to be “a process of normative aging” but according to the International Classification of Disease, Tenth Revision, Clinical Modification (ICD-10-CM), as a disease. As sarcopenia is an ineluctable process, prevention and management are the only options to promote healthy aging; these actions should perhaps be taken during youth. Included in this book: · Features essential information on sarcopenia, its current definition, and molecular and cellular aspects of this disease · Discusses the development of physical frailty, a complication of sarcopenia, and predicts its occurrence in the older population · Presents alterations in muscle protein turnover and mitochondrial dysfunction in the aging process · Provides data on the negative involvement of sarcopenia in certain chronic diseases · Describes presbyphagia or age-related changes in the swallowing mechanism in older people · Details possible strategies to combat muscle wasting in healthy older adults and their limits This book features information collected from pioneers or experts on human aging from around the globe, including Europe, Brazil, Canada, Japan and the United States. It is a valuable source of information for nutritional scientists, medical doctors, sports scientists, food scientists, dietitians, students in these fields, and for anyone interested in nutrition. We hope this book provides a better understanding of sarcopenia which inevitably occurs with aging without weight loss. Moreover, this book will supply information outlining strategies to prevent or limit muscle wasting due to normal aging in order to promote successful aging.

This book aims to present the age-related alterations in redox signaling networks and their diagnostic biomarkers in aging cells using multidisciplinary approach. Establishing sensitive and specific biomarkers of dynamic redox homeostasis is crucially important in the development of effective antiaging and senolytic interventions. Recent years have seen tremendous advances in the understanding of redox signaling events which highlight the process of aging and age-related pathologies. A major challenge in biological aging research is developing reliable biomarkers to determine the consequences of disrupted redox signaling networks long before the clinical diagnosis of age-related diseases is made. Therefore, we have chosen to concentrate on aging-induced aberrant redox signaling networks, their biomarkers, and pathological consequences in this book. Although oxidation is a natural metabolic process, the imbalance in the level of oxidants and antioxidants causes oxidative stress and eventually leads to inflammatory conditions, diabetes, neurodegenerative diseases, and cancer. Novel redox-sensitive biomarkers for the evaluation of aging-induced proteinopathies such as amyloid ß and tau proteins in Alzheimer's disease, α-synuclein in Parkinson's disease, and islet amyloid polypeptides in type 2 diabetes mellitus recently drew the attention of researchers. Inside this textbook, readers will find comprehensive perspectives on the association between redox homeostasis and the aging process both at the molecular and clinical levels. Due to the inherent relationship between impaired metabolic activities and oxidative stress, the temporal interaction between intermediary metabolism and disturbed redox status can lead to greater susceptibility to aging-induced diseases and disorders, such as cardiovascular diseases, hypertension, and diabetes. This knowledge could be a key to continued research toward improving medication regimens such as in cancer and cardiovascular therapies, and procedural outcomes for patients. This book brings together current research evidence and knowledge on redox signaling and biomarkers in aging in chapters written by leading global experts in this rapidly evolving field. We hope that this textbook is of interest to a wide group of researchers, advanced students, scientifically curious non-specialist readers and clinicians alike.