Cells, Aging, and Human Disease is the first book to explore aging all the way from genes to clinical application, analyzing the fundamental cellular changes which underlie human age-related disease. With over 4,000 references, this text explores both the fundamental processes of human aging and the tissue-by-tissue pathology, detailing both breaking research and current state-of-the-art clinical interventions in aging and age-related disease. Far from merely sharing a common onset late in the lifespan, age-related diseases are linked by fundamental common characteristics at the genetic and cellular levels. Emphasizing human cell mechanisms, the first section presents and analyzes our current knowledege of telomere biology and cell senescence. In superb academic detail, the text brings the reader up to date on telomere maintenance, telomerase dynamics, and current research on cell senescence--and the general model--cell senescence as the central component in human senescence and cancer. For each human malignancy, the chapter reviews and analyzes all available data on telomeres and telomerase, as well as summarizing current work on their clinical application in both diagnosis and cancer therapy. The second edition, oriented by organs and tissues, explores the actual physiological impact of cell senescence and aging on clinical disease. After a summary of the literature on early aging syndromes--the progerias--the text reviews aging diseases (Alzheimer's dementia, osteoarthritis, atherosclerosis, immune aging, presbyopia, sarcopenia, etc.) in the context of the tissues in which they occur. Each of the ten clinical chapters--skin, cardiovascular system, bone and joints, hematopoetic and immune systems, endocrine, CNS, renal, muscle, GI, and eyes--examines what we know of their pathology, the role of cell sensescence, and medical interventions, both current and potential.
Why do we age? Is aging inevitable? Will advances in medical knowledge allow us to extend the human lifespan beyond its present limits? Because growing old has long been the one irreducible reality of human existence, these intriguing questions arise more often in the context of science fiction than science fact. But recent discoveries in the fields of cell biology and molecular genetics are seriously challenging the assumption that human lifespans are beyond our control. With such discoveries in mind, noted cell biologist William R. Clark clearly and skillfully describes how senescence begins at the level of individual cells and how cellular replication may be bound up with aging of the entire organism. He explores the evolutionary origin and function of aging, the cellular connections between aging and cancer, the parallels between cellular senescence and Alzheimer's disease, and the insights gained through studying human genetic disorders--such as Werner's syndrome--that mimic the symptoms of aging. Clark also explains how reduction in caloric intake may actually help increase lifespan, and how the destructive effects of oxidative elements in the body may be limited by the consumption of antioxidants found in fruits and vegetables. In a final chapter, Clark considers the social and economic aspects of living longer, the implications of gene therapy on senescence, and what we might learn about aging from experiments in cloning. This is a highly readable, provocative account of some of the most far-reaching and controversial questions we are likely to ask in the next century.
Aging represents a physiological and per se non-pathological and multifactorial process involving a set of key genes and mechanisms being triggered by different endogenous and exogenous factors. Since aging is a major risk factor in connection with a variety of human disorders, it is increasingly becoming a central topic in biochemical and medical research. The plethora of theories on aging – some of which have been discussed for decades – are neither isolated nor contradictory but instead can be connected in a network of pathways and processes at the cellular and molecular levels. This book summarizes the most prominent and important approaches, focusing on telomeres, DNA damage and oxidative stress as well as on the possible role of nutrition, the interplay between genes and environment (epigenetics) and intracellular protein homeostasis and introduces some genes that have actually extended life spans in animal models. Linking these different determinants of aging with disease, this volume aims to reveal their multiple interdependencies. We see that there is no single “perfect” theory of aging and that instead it is possible to define what the authors call the molecular aging matrix of the cell. A better knowledge of its key mechanisms and the mutual connections between its components will lead to a better understanding of age-associated disorders such as Alzheimer’s disease.
Cellular AGING AND CELL DEATH Edited by Nikki J. Holbrook, George R. Martin, and Richard A. Lockshin Cellular Aging and Cell Death provides a thorough understanding of the mechanisms responsible for cellular aging, covering the recent research on programmed cell death and senescence, and describing their role in the control of cell proliferation and the aging process. This one-of-a-kind book is the first to combine the two hottest research areas of cell biology into one comprehensive text. Leading experts contribute to give readers an authoritative overview of the distinct fields of cellular aging and programmed cell death, as well as to demonstrate how both fields are critical to understanding the aging process. They address the large and growing interest in apoptosis, especially with regard to the molecular signals that induce and regulate programmed cell death, and the role of apoptosis in a variety of age-associated diseases and disabilities. Throughout the book, a strong emphasis is placed on the interrelationship of the molecular, cellular, and physiological aspects of senescence. Individual chapters discuss such topics as the role and regulation of apoptosis in development, the potential impact of cell death on such postmitotic tissues as nerve and muscle, and suggest that programmed cell death plays an important role in both pathological and nonpathological aspects of aging, including neurodegenerative diseases. One important chapter focuses on the most recent research involving the study of telomeres, whose reduction in length with age and cell division may underlie cellular senescence. The subject of neuronal cell death is also put into the perspective of aging. Cellular Aging and Cell Death bridges the rapidly growing fields of cellular aging and programmed cell death. This thorough, yet concise book will be of particular interest to graduate students and researchers within the fields of cell and developmental biology, neurobiology, immunology, and physiology. Physicians and medical students involved in the fields of gerontology and pathology will also find this an informative reference.
Robert Arking's Biology of Aging, 3rd edition, is an introductory text to the biology of aging which gives advanced undergraduate and graduate students a thorough review of the entire field. His prior two editions have also served admirably as a reference text for clinicians and scientists. This new edition captures the extraordinary recent advances in our knowledge of the ultimate and proximal mechanisms underlying the phenomenon of aging. As a result, six important conceptual changes are included here: ? Clarified distinctions between the biological mechanisms involved in longevity determination and those involved in senescent processes. ? A new conceptual framework around which we can organize all the new facts about aging. This will assist readers to make sense of the information and use the data to form their own ideas. ? Increased knowledge of aging cells has lead to new ideas on how a cell transits from a healthy state to a senescent state, while still allowing for high levels of intra- and inter-specific variability. ? Discussion of senescent mechanisms assists the reader to understand that aging is a non-programmatic loss of function, likely arising from the loss of regulatory signals, and so is modifiable in the laboratory. ? Because the standard evolutionary story does not fully explain the evolution of social organisms, this edition also includes recent work dealing with intergenerational resource transfers. ? Lastly, if aging mechanisms are plastic, then the demand to move these anti-aging interventions into the human arena will inevitably grow. A discussion of the biological and ethical arguments on both sides of the question frames the question in an appropriate manner. The mass of data related to aging is summarized into fifteen focused chapters, each dealing with some particular aspect of the problem. The last two chapters integrate all this material into a coherent view of how the relevant biological processes change over the life span. This view is expressed in two non-technical figures (you might say that the whole book exists to fully support Figs 9-4 & 14-9), whose meanings are elucidated as the reader progresses through the book.
This book brings together some of the best researchers in the field of aging and neurodegenerative diseases and presents up-to-date information concerning new developments in this exciting area of research in quite separate fields of biomedical science. It includes a wide range of issues such as basic and applied concepts, methods, and techniques used in this area. The chapters examine and evaluate our understanding of the pathogenetic mechanisms involved in these fields such as increased protein oxidation and macromolecular modifications associated with aging. This is a novel strategy for the visualization of ROS-induced protein oxidation and protection by antioxidants in living cells using fluorescent probes, thermochemiluminescence (TCL) methodology for determination of the oxidative status of biological systems in experimental and clinical setups, protein degradation, proteasome inactivation observed in the aging process or caused by oxidative stress. Other topics addressed are the oxidative stress theory of aging, oxidation and removal of protein aggregates in neurodegeneration, causes and consequences of oxidative stress in Alzheimers disease, assessment of antioxidants as a therapeutic for neurodegenerative diseases, rafts and prions, the many forms of the prion protein and its subcellular pathways, signaling pathways in protection of neural tissues by ischemic and drug-induced preconditioning, folding of proteins associated with neurodegenerative disorders and aging and neuroprotection in immuno-mediated neurodegeneration from infection to autoimmunity.
Ageing has become a great problem for many countries. Due to world-wide life prolongation the number of people over 6o years old has grown rapidly into a ten percent piece of the world population. The growing age of the world population raises many social, economical, and medical problems. The proportion of people in the economically active age groups to those who are over 65 is constantly decreasing. A major consequence of the increasing numbers of individuals in advanced age groups is increasing numbers of patients suffering from age-related diseases. The aim of this book is to present the basic data on human ageing as well as on age-related diseases.
Extensively revised and updated to reflect the current state of knowledge in the study of aging, this Fourth Edition offers a complete profile of the aging process at all levels, from molecules and cells to demography and evolution. Written by international experts in current basic and clinical aging research, this text includes aspects of individual, comparative, and differential aging, and discussions of theories and mechanisms of aging. This invaluable reference illustrates how bodily systems, organs, and functions are affected with aging, describes how genetic and environmental factors influence age-related changes, and addresses some of the clinical consequences of these changes for health and longevity. Well illustrated, with numerous tables and graphs, this book presents up-to-date information from internationally renowned experts in various bio-medical fields. New updated information includes: emphasis on emerging technologies and recent advances in biology and bioengineering that allow greater and longer independence of the elderly recent therapeutic developments in key diseases such as Alzheimer's, osteopenia, osteoporosis, high cholesterol, diabetes, gastritis, sexual impotence, and using transgenic animals as models of aging evaluation of the latest knowledge on the roles of oxidants and antioxidants, and correlates them with other aging-based theories expanded discussion of nutrition and physical exercise chapters on gene and stem cell interventions related to the aging process updated tables to reflect current trends, new research data, and up-to-date statistical information
One of Wall Street Journal’s "Best Books for Science Lovers" in 2015 Science is on the cusp of a revolutionary breakthrough. We now understand more about aging—and how to prevent and reverse it—than ever before. In recent years, our understanding of the nature of aging has grown exponentially, and dramatic life extension—even age reversal—has moved from science fiction to real possibility. Dr. Michael Fossel has been in the forefront of aging research for decades and is the author of the definitive textbook on human aging. In The Telomerase Revolution, he takes us on a detailed but highly accessible scientific journey, providing startling insights into the nature of human aging. Twenty years ago, there was still considerable debate of the nature of human aging, with a variety of competing theories in play. But scientific consensus is forming around the telomere theory of aging. The essence of this theory is that human aging is the result of cellular aging. Every time a cell reproduces, its telomeres (the tips of the chromosomes) shorten. With every shortening of the telomeres, the cell’s ability to repair its molecules decreases. It ages. Human aging is the result of the aging of the body’s trillions of cells. But some of our cells don’t age. Sex cells and stem cells can reproduce indefinitely, without aging, because they create telomerase. Telomerase re-lengthens the telomeres, keeping these cells young. The Telomerase Revolution describes how telomerase will soon be used as a powerful therapeutic tool, with the potential to dramatically extend life spans and even reverse human aging. Telomerase-based treatments are already available, and have shown early promise, but much more potent treatments will become available over the next decade. The Telomerase Revolution is the definitive work on the latest science on human aging, covering both the theory and the clinical implications. It takes the reader to the forefront of the upcoming revolution in human medicine.
The proportion of elderly people continues to increase in the western world-nearly a quarter of the population will be over 65 years by the year 2050. Since aging is accompanied by an increase in diseases and by a deterioration in well-being, finding solutions to these social, medical and psychological problems is necessarily a major goal for society. Scientists and medical practitioners are therefore faced with the urgent task of increasing basic knowledge of the biological processes that cause aging. More resources must be put into this research in order to achieve better understanding of the cellular mechanisms that underlie the differences in life span between species and to answer the difficult questions of why some individuals age more quickly than others, and why some develop liver problems, some have heart problems, and others brain problems. The results of such a wide program of research will provide important information about the causes of many life-threatening and/ or debilitating diseases of old age; it will help find ways to prevent some of the ailments that result from aging, and it may well lead to discoveries enabling the prolongation of human life.