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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.
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.
Featuring extensive references, updated for this paperback edition, Longevity, Senescence, and the Genome constitutes a landmark contribution to biomedicine and the evolutionary biology of aging. To enhance gerontology's focus on human age-related dysfunctions, Caleb E. Finch provides a comparative review of all the phyla of organisms, broadening gerontology to intersect with behavioral, developmental, evolutionary, and molecular biology. By comparing species that have different developmental and life spans, Finch proposes an original typology of senescence from rapid to gradual to negligible, and he provides the first multiphyletic calculations of mortality rate constants.
The Biology of Senescence
Genome Stability: From Virus to Human Application, Second Edition, a volume in the Translational Epigenetics series, explores how various species maintain genome stability and genome diversification in response to environmental factors. Here, across thirty-eight chapters, leading researchers provide a deep analysis of genome stability in DNA/RNA viruses, prokaryotes, single cell eukaryotes, lower multicellular eukaryotes, and mammals, examining how epigenetic factors contribute to genome stability and how these species pass memories of encounters to progeny. Topics also include major DNA repair mechanisms, the role of chromatin in genome stability, human diseases associated with genome instability, and genome stability in response to aging. This second edition has been fully revised to address evolving research trends, including CRISPRs/Cas9 genome editing; conventional versus transgenic genome instability; breeding and genetic diseases associated with abnormal DNA repair; RNA and extrachromosomal DNA; cloning, stem cells, and embryo development; programmed genome instability; and conserved and divergent features of repair. This volume is an essential resource for geneticists, epigeneticists, and molecular biologists who are looking to gain a deeper understanding of this rapidly expanding field, and can also be of great use to advanced students who are looking to gain additional expertise in genome stability. - A deep analysis of genome stability research from various kingdoms, including epigenetics and transgenerational effects - Provides comprehensive coverage of mechanisms utilized by different organisms to maintain genomic stability - Contains applications of genome instability research and outcomes for human disease - Features all-new chapters on evolving areas of genome stability research, including CRISPRs/Cas9 genome editing, RNA and extrachromosomal DNA, programmed genome instability, and conserved and divergent features of repair
The release of the complete version of the human genome sequence in 2003 has paved the way for defining gene function and genetic background for phenotypic variation in humans and allowed us to study the aging process in a new light. This new volume results from that research and focuses on the genetic and epigenetic process of aging. While the interpretation of the genome data is still in its initial stages, this new volume looks at the evolving understanding of molecular mechanisms involved in cellular processes, gene function associated with complex traits, epigenetic components involve in gene control and the creation of hypothesis-free genome-wide approaches. Longevity Genes: A Blueprint for Aging explores the genetic and genomic elements that can maintain a long life such as DNA damage mechanisms, epigenetics and the way we can use this knowledge to generate customized treatments. It touches on some of the multidisciplinary approaches as well as genomic-wide association technology used to analyze complex traits. This book describes the hunt for genes affecting complex traits using a high throughput technology, with adequate consideration for the selection of an appropriate population, applications of statistical genetics and computational biology, and most importantly, considering phenotype-genotype association studies. Longevity Genes provides coverage of not only established aspects of genetics and aging, but also new approaches and perceptions in this important area of research.
The aim of volume 7 of Human Cell Culture is to provide clear and precise methods for growing primary cultures of adult stem cells from various human tissues and describe culture conditions in which these adult stem cells differentiate along their respective lineages. The book will be of value to biomedical scientists and of special interest to stem cell biologists and tissue engineers. Each chapter is written by experts actively involved in growing human adult stem cells.
Why do we age? The answer to this question is critical to our ability to prevent and treat highly age-related diseases such as cancer and heart disease that now cause the deaths of most people in the developed world. This short book provides an overview of biological aging theories including history, current status, major scientific controversies, and implications for the future of medicine. Major topics include: human mortality as a function of age, aging mechanisms and processes, the programmed vs. non-programmed aging controversy, empirical evidence on aging, and the feasibility of anti-aging and regenerative medicine. Evolution theory is essential to aging theories. Theorists have been struggling for 150 years to explain how aging, deterioration, and consequent death fit with Darwin’s survival of the fittest concept. This book explains how continuing genetics discoveries have produced changes in the way we think about evolution that in turn lead to new thinking about the nature of aging.
"Theoretical biologist Josh Mitteldorf and ... ecological philosopher Dorion Sagan [posit] that evolution and aging are even more complex and breathtaking than we originally thought. Using ... multidisciplinary science, as well as reviewing the history of our understanding about evolution, this book makes the case that aging is not something that 'just happens, ' nor is it the result of wear and tear or a genetic inevitability. Rather, aging has a fascinating evolutionary purpose: to stabilize populations and ecosystems, which are ever-threatened by cyclic swings that can lead to extinction"--
"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