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"How long can humans live? Is immortality possible? Just what is the aging process? The aging and inevitable death of the human body have inspired more myths and outrageous quackery than anything else subject to scientific inquiry. . . . Now comes a most fascinating book, insightful and scholarly, to provide what answers have emerged so far." --San Francisco Chronicle Here, at last, preeminent cell biologist Leonard Hayflick presents the truth about human aging. Based on more than thirty years of pioneering research in the field, How and Why We Age explores not only how our major biological systems change as we grow older, but also examines the intangible alterations in our modes of thinking and feeling, our moods and sexual desires, our personality traits and our memories. With the immediacy of the latest scientific discoveries, Dr. Hayflick explains how aging affects every part of the body, and dispels many of the most persistent aging myths, to show that: * Hearts do not naturally get weaker with age. * Regular exercise and a low-fat diet won't slow aging. * Curing cancer would only add two years to the average sixty-five-year-old American life. Curing heart disease, however would add fourteen years. * Only five percent of people over the age of sixty-five are in nursing homes * No human has lived--or probably can live--past 120 years. Gracefully written, clearly organized, and packed with essential facts and statistics, How and Why We Age is a landmark study of the aging process for readers of all ages. "Written in clear, nontechnical language, it is an excellent introduction to the scientific and demographic literature on this multifacetedsubject." --Nature
Aging has long since been ascribed to the gradual accumulation of DNA mutations in the genome of somatic cells. However, it is only recently that the necessary sophisticated technology has been developed to begin testing this theory and its consequences. Vijg critically reviews the concept of genomic instability as a possible universal cause of aging in the context of a new, holistic understanding of genome functioning in complex organisms resulting from recent advances in functional genomics and systems biology. It provides an up-to-date synthesis of current research, as well as a look ahead to the design of strategies to retard or reverse the deleterious effects of aging. This is particularly important in a time when we are urgently trying to unravel the genetic component of aging-related diseases. Moreover, there is a growing public recognition of the imperative of understanding more about the underlying biology of aging, driven by continuing demographic change.
The ?eld of cellular responses to DNA damage has attained widespread recognition and interest in recent years commensurate with its fundamental role in the ma- tenance of genomic stability. These responses, which are essential to preventing cellular death or malignant transformation, are organized into a sophisticated s- tem designated the “DNA damage response”. This system operates in all living organisms to maintain genomic stability in the face of constant attacks on the DNA from a variety of endogenous by-products of normal metabolism, as well as exogenous agents such as radiation and toxic chemicals in the environment. The response repairs DNA damage via an intricate cellular signal transduction network that coordinates with various processes such as regulation of DNA replication, tr- scriptional responses, and temporary cell cycle arrest to allow the repair to take place. Defects in this system result in severe genetic disorders involving tissue degeneration, sensitivity to speci?c damaging agents, immunode?ciency, genomic instability, cancer predisposition and premature aging. The ?nding that many of the crucial players involved in DNA damage response are structurally and functionally conserved in different species spurred discoveries of new players through similar analyses in yeast and mammals. We now understand the chain of events that leads to instantaneous activation of the massive cellular responses to DNA lesions. This book summarizes several new concepts in this rapidly evolving ?eld, and the advances in our understanding of the complex network of processes that respond to DNA damage.
This book investigates the various processes that are affected by the age of an organism. Several new tools for the analysis of biological aging have been introduced recently, and this volume provides methods and protocols for these new techniques in addition to its coverage of established procedures. Researchers seeking new technology and techniques will find this volume of tremendous benefit as they move towards new directions.
Recent studies have indicated that epigenetic processes may play a major role in both cellular and organismal aging. These epigenetic processes include not only DNA methylation and histone modifications, but also extend to many other epigenetic mediators such as the polycomb group proteins, chromosomal position effects, and noncoding RNA. The topics of this book range from fundamental changes in DNA methylation in aging to the most recent research on intervention into epigenetic modifications to modulate the aging process. The major topics of epigenetics and aging covered in this book are: 1) DNA methylation and histone modifications in aging; 2) Other epigenetic processes and aging; 3) Impact of epigenetics on aging; 4) Epigenetics of age-related diseases; 5) Epigenetic interventions and aging: and 6) Future directions in epigenetic aging research. The most studied of epigenetic processes, DNA methylation, has been associated with cellular aging and aging of organisms for many years. It is now apparent that both global and gene-specific alterations occur not only in DNA methylation during aging, but also in several histone alterations. Many epigenetic alterations can have an impact on aging processes such as stem cell aging, control of telomerase, modifications of telomeres, and epigenetic drift can impact the aging process as evident in the recent studies of aging monozygotic twins. Numerous age-related diseases are affected by epigenetic mechanisms. For example, recent studies have shown that DNA methylation is altered in Alzheimer’s disease and autoimmunity. Other prevalent diseases that have been associated with age-related epigenetic changes include cancer and diabetes. Paternal age and epigenetic changes appear to have an effect on schizophrenia and epigenetic silencing has been associated with several of the progeroid syndromes of premature aging. Moreover, the impact of dietary or drug intervention into epigenetic processes as they affect normal aging or age-related diseases is becoming increasingly feasible.
Aging occurs at the level of individual cells, a complex interplay between intrinsic "programming" and exogenous "wear and tear", with genetically-determined cellular capacity to repair environmentally-induced DNA damage playing a central role in the rate of aging and its specific manifestations. In 12 chapters, "The Role of DNA Damage and Repair in Cell Aging" provides an intellectual framework for aging of mitotic and post-mitotic cells, describes a variety of model systems for further studies, and reviews current concepts of DNA responses and their relationship to the phenomenon of aging. As part of a series entitled "Advances in Cell Aging and Gerontology," this volume also summarizes seminal recent discoveries such as the molecular basis for Werner syndrome (a mutant DNA helicase), the complementary roles of telomere shortening and telomerase activity in cell senescence versus immortalization, the role of apoptosis in the homeostasis of aging tissue, and the existence of an inducible SOS-like response in mammalian cells that minimizes DNA damage from repeatedly encountered injurious environmental agents. Insights into the relationship between cellular aging and age-associated diseases, particularly malignancies, are also provided in several chapters. This book is an excellent single source of information for anyone interested in DNA repair, mechanisms of aging, or certainly their intersection. Students will gain a general appreciation of these fields, but even the most senior investigators will benefit from the detailed coverage of rapidly advancing areas.
Why organisms age and why sexual reproduction exists are major unsolved problems in biology. This book provides an integrated explanation of aging and sex based on current knowledge of DNA damage and repair. - Discusses the universality of the problem of DNA damage - Describes aging as a consequence of accumulated DNA damage - Considers meiosis as an adaptation for DNA repair - Discusses mating in eukaryotes as an adaptation for masking mutation
The Genetics of Aging is divided into several sections in an attempt to provide a logical progression from the level of the genome to the realm of human genetics. The relationship between the genetic material and aging will be thoroughly explored in the initial chapters. These chapters discuss in depth the various theories that have been proposed for the mechanisms of aging at the molecular level and present data which either support or contradict these hypotheses. Subsequent chapters will deal with the genetics of aging in organisms ranging from paramecium to mammals. The largest section of this volume will be devoted to several important areas in human genetics: human genetic disorders which feature premature aging, the effect of human parental aging on the production of genetically abnor mal offspring, the genetics of human longevity, and a review of studies on aging human twins. Over the last few decades genetic technology has provided enormous insight into a number of disciplines. Therefore, in the last few chapters, several genetic approaches to the study of aging are discussed: somatic cell genetics, immunogenetics, and behavioral genetics. As the goal of this volume is to present a comprehensive examination of the genetics of aging, most chapters are oriented toward general review of their respective areas. It is my hope that this volume will encourage clinical, biological, and behavioral investigators to turn their attention to the genetic aspects of aging as well as to employ genetic technology to obtain further insight into aging processes.
This book illustrates the activities of mammalian sirtuin SIRT6 in connection with DNA damage repair and premature aging. It mainly presents research on the nuclear lamin A, notably the upregulation of p53 and acetylation etc. Taken together, these studies reveal the various regulatory roles of SIRT6, which are of substantial biological relevance in DNA damage repair, aging and longevity, and can have significant implications in devising therapeutic strategies to combat age-associated pathologies. Given its scope, the book offers a valuable resource for students and researchers in the fields of genetics, cell biology, molecular biology etc.
The overall aim of these books is to give scientists in academia and industry a comprehensive overview of the field of DNA damage and DNA repair and related human diseases.