Aging of the Genome: The Dual Role of DNA in Life and Death

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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.

A Means to an End: The Biological Basis of Aging and Death

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An easy book to read
A good review with some problems
Yes, death is genetically programmed !
A clear explanation of what is currently known about aging
The case for programmed senescence

A Means to an End: The Biological Basis of Aging and Death
William R. Clark
Manufacturer: Oxford University Press, USA
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ASIN: 0195153758

Book Description

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.

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An easy book to read.......2003-08-20

Easy to read book. After lengthy introduction author concentrates on the research about genes that suppress the cell senescence and control. Discussion about cancer cells where cell division is not checked.
Final chapters discusses the effects of oxidants, obesity, low calorie diet or similar things where eventually a claim comes that beside the gene control everything else does not amount more than %15 in total effect.
So unless we control the genes we will soon or later die.

A good review with some problems.......2002-02-04

Dr. Clark provides a good review of the field but fails, in my opinion, to provide a clear explanation for "The biological basis of aging and death". The theories of the evolutionary biology of aging clearly argue that "aging" cannot be "genetically programmed" or that "We are programmed to grow old and die" as other reviewers have concluded from reading this work. That points out the weakness in this book -- a failure to clearly differentiate between senescence, aging and death. There are two primary theories for why we age -- "the declining force of natural selection" (i.e. it is difficult to optimize a genetic program to produce non-aging organisms) and "antagonistic plieotropy" (i.e. the genetic program is optimized for reproduction at the expense of non-aging longevity). Dr. Clark seems to suggest that the genetic program for senescence is what causes aging and death. In fact the genetic program for senescence is largely an anti-cancer program. It may as a side effect contribute to aging and eventually death but its primary purpose is to prevent cancer. There is a very big difference between saying that aging and death result from an "incomplete" program and saying that aging and death result from a pre-programmed senescence program. One of my primary criticisms is Dr. Clark's pseudo-deathist philosophy. The tone of the book seems to suggest that aging is pre-programmed and cannot be changed. He says, on pg 218, "Will we want to go this far in our search for the fountain of youth? It is unlikely even to be proposed in the lifetime of anyone reading this book, but it is not at all beyond the realm of possibility." (He is speaking of the application of gene therapies to lifespan extension.) I have been proposing such methods for lifespan extension for most of the past decade and have conducted research and founded companies to forward these goals. The human genome is a program. It has bugs in it that result in aging. We can comprehend those bugs and apply patches to fix them allowing the extension of human longevity to the accident-rate limits which will be thousands of years. Individuals who really want to understand aging should read books by people who have studied the field for many years. The best authors, in my opinion, would be Steve Austad, Tom Kirkwood and Caleb Finch. While many of their works may be older than this book, they have a greater depth of understanding of the subtleties of the study of aging that this book fails to discuss.

Yes, death is genetically programmed !.......2000-08-13

This book embraces a rational and well explained journey in the field of aging. Here I read for the first time strong statements about the programmed nature death, that is present since fertilization. We learn the basic experiments that support Haldane theory about sex and aging and we appreaciate the beatiful connection between replicative senescence and species-specifc mortality. The book is clear and well readible and I strongly recommend it to science and non-science crowd.

A clear explanation of what is currently known about aging.......2000-06-12

Professor Clark has written a book that is detailed and accurate, and at the same time accessible to people untrained in molecular biology. If you are interested in increasing both the quality and the length of your life, read this book.

The case for programmed senescence.......2000-05-14

Professor Clark writes with elegance and employs a reasoned tone, but he is not always direct, and often expresses ideas in the understandably tentative way of a very exacting scientist. Consequently it is not easy to see that nowhere in this book does he directly say what causes aging and death. Nor does he simply say we don't know. What he does say is there are some persuasive theories, especially the evolutionary model began by Haldane and Medawar and refined by George Williams (pp. 49-50), that are consistent with the data that "may be essentially correct, at least in broad outline." (p. 52). Clark makes it clear that we have senescence effector genes in our cells but he doesn't say how they got there, only that they were "already in place in the earliest eukaryotic organisms such as paramecia and yeast." (p. 57) The reader is left to believe that there is a mechanism that retains them, but what that mechanism might be is unclear.

I am led to believe that senescence is built into our cells and is part of our genetic makeup. We are programmed to grow old and die. Just how is what Professor Clark is exploring here. He concentrates on the cellular level because it is his belief that this is where the mechanisms for senescence can be found. On page 190 he argues that senescence is genetically controlled and not the result of a random breakdown, citing the fact that "maximum lifespan is species-specific." In short, humans live a lot longer than dogs, contrary to what might be expected if senescence were caused by cells getting old and wearing out. He points out on page 48 that "mice and humans, although composed of proteins that are extremely similar at a chemical level, have both average and maximal lifespans differing by a factor of 30 or more."

Clark also covers in some detail such issues as the evolution of senescence, average and maximum lifespan; genetic diseases such as Werner's syndrome, the Hutchinson-Gilford syndrome and others; oxidative stress as a cause of cellular senescence and the use of Vitamin E and other antioxidants; the aging brain and Alzheimer's disease; cancer and the social and economic effect of humans living longer. A chapter is devoted to the phenomenon of increased lifespan through restricted caloric intake.

Book Description

Apoptosis, or programmed cell death, is a natural process by which damaged or unwanted cells are dismantled in an orderly and atraumatic fashion. It is of critical importance in development, homeostasis, and cell population control. Research over the last decade is now enabling scientists to comprehend how genes and the protein products interact to control apoptosis. This has led to the current position where researchers may be able to directly modify the action of key proteins through gene therapy and antisense oligonucleotides.
Apoptosis Genes presents a current overview of key genes involved in the control of apoptosis research together with thoughts on future prospects and clinical applications. While there are several books written on apoptosis, Apoptosis Genes deals specifically with the regulation of apoptosis. Given the increased interest in the role of apoptosis genes in disease processes, this work will be useful to researchers investigating cancer, autoimmune disease, viral infection, cardiovascular disease, neurodegenerative disorders, AIDS, osteoporosis, and aging.

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Apoptosis in Toxicology

Manufacturer: CRC
ProductGroup: Book
Binding: Hardcover

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ASIN: 0748408150

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Apoptosis in Toxicology is the first book to focus on the molecular regulation of apoptosis with particular emphasis on toxicant action. Cell survival signalling and its perturbation is addressed at the genetic and biochemical level, including key survival and death genes, survival signalling, commitment to apoptosis and recruitment of the initiator and executioner caspases. Emphasis is given to the role apoptosis plays in the action of toxicants in the brain, the immune system, the reproductive organs, the kidney and the liver. The ability of drugs to regulate apoptosis either as a target or as an adverse effect is discussed with particular reference to cancer chemotherapy. The many methods that can be employed to quantify apoptosis are compared and their application to different tissues is discussed. This timely and comprehensive volume has been written by leading authorities and active researchers in their respective fields. It will have broad appeal to toxicologists, physicians and biologists across many disciplines.

Apoptotic Pathways as Targets for Novel Therapies in Cancer and Other Diseases

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Apoptotic Pathways as Targets for Novel Therapies in Cancer and Other Diseases

Manufacturer: Springer
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Binding: Hardcover

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ASIN: 0387233849

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As our understanding of apoptotic pathway expands, we are coming to realize the great potential of utilizing this pathway to treat diseases such as cancer. The book attempts to review, summarize, and speculate on the apoptotic pathways, how are they regulated and how targeted therapies are being used to treat a wide variety of diseases. Special emphasis is placed on cancer since new treatments either being developed or currently in the clinical setting are showing great promise to increase survival rates for cancer patients. Chapters will address the biology behind regulating the apoptotic pathways and what goes wrong in disease states whereas other chapters will concentrate on new therapies targeting apoptotic pathways. The reader by the end of the book should have greater insight into the understanding and utilization of apoptotic pathways to fight diseases such as cancer.

Cell Apoptosis: Regulation and Environmental Factors

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Cell Apoptosis: Regulation and Environmental Factors

Manufacturer: Nova Science Publishers Inc
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Binding: Hardcover

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ASIN: 1600215084

Cell Injury (Principles of Medical Biology)

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Cell Injury (Principles of Medical Biology)

Manufacturer: Elsevier Science
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ASIN: 1559388188

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At no time since the introduction of cell pathology by Virchov more than a century ago has the outlook for pathology as an integrated discipline been brighter. It is surely clear that the revolution of molecular biology and biotechnology has wrought profound changes in the various basic medical sciences including pathology. But to say this is hardly enough, particularly since the burgeoning field of molecular pathology has been challenged and altered by a powerful concept, namely, programmed cell death. Called apoptosis, which in Greek means falling off, it is intimately connected with cell removal and regeneration; that is, with tissue homeostasis. Nowhere is this more dramatically illustrated as a physiological process than in the gut, endometrium, and embryo. Similarly, little doubt is left that clusters of apoptotic-induced genes are involved in the control of carcinogenesis. The evidence for this is already compelling; it is plain, for instance, that p53 triggers apoptosis whenever DNA repair is incomplete. The question now is, how quickly can the Genome project shed some light on the genetics underlying apoptosis?
It is tolerably clear that there is no such thing as a general model of cell injury, but there are models, as it should be. One thing is already certain: cell stress during septicemia is the quintessential model. Death here requires the failure of at least three organs! We are told that oxidative stress plays a major role in the pathogenesis of the syndrome. This is not surprising. The whole subject of reactive oxygen species (ROS) is thus given much weight. By far, the most important mechanisms underlying membrane lesions, due to ROS, are those involving inactivation of several key enzymes among a host of enzymes, lipid peroxidation, and iron speeding up bydroxyl radical production. The stark fact is that evolutionary pressure has produced a fiasco by not endowing the cell with enough antioxidant power or reducing the ROS pool. In organs with high O2 consumption, mitochondrial leakage of O2 (the superoxide anion) could well be considerable. Thus our main point here is that caloric restriction gives us a way of tackling the problem for the time being. One has only to remember that it improves survival.
Whether there has been a "breakthrough" is not yet quite certain, but oxidative stress combined with long-term overactivation of glutamate receptors may enable us to understand several neurodegenerative disorders including Parkinson's disease. This broad topic is touched upon in detail in the Neurobiology module (Volume 14).
There is a vast literature relating to injury of heart muscle. Two chapters address this topic. Looking back, are we to conclude that a membrane lesion, which is essentially functional, does not exist? Consider, as an example, the NMR experiments in which a raised Pco2, leads very rapidly to a fall in heart muscle pH. We also venture whether it begs several fundamental questions relating to events that precede the onset of necrobiosis. A telling argument is that an early event could be as simple as the root of the problem in ischemia is not as simple as that of a leaky membrane. But the initiating event would seem to be a redox imbalance vix., changes in cytosolic and mitochondrial NAD+/NADH.
We urge the student to go back to Volume 4 (Part II) and read, once more, the chapter on Cellular ATP by Harris. In Part IV, the chapter on the Human Heat Shock Response by Jurivich merits a second reading. Though the present volume is a veritable source of many unanswered questions, it has the distinct simplicity of telling us that molecular pathology, like molecular biology, represents a way of thinking.

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Fungal Genomics (The Mycota)

Manufacturer: Springer
ProductGroup: Book
Binding: Hardcover

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ASIN: 354025594X

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Through the integration of bioinformatic, genetic, transcriptomic, proteomic, metabolomic, phenomic and other massive datasets, genomics is revealing exciting new insights into fungal cell biology. The central theme of this volume is the strong impact that genomics is having upon our understanding of fungal biology, across a wide range of species, including model yeasts (such as Saccharomyces cerevisiae and Schizosaccharomyces pombe), filamentous fungi (such as Neurospora crassa and Aspergillus nidulans) and pathogenic fungi (such as Magnaporthe grisae, Candida albicans, Cryptococcus neoformans and Histoplasma capsulatum). World-renowned scientists address the following topics in these fungi: systems biology and evolution, circadian rhythms, apoptosis and stress responses, secretion, and environmental signalling networks. Particular emphasis is placed on fungal pathogenicity. Various genomic technologies are discussed, including genome-wide sequence comparisons, transcript profiling, proteomics, metabolomics and bioinformatics.

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Genetics of Apoptosis

Manufacturer: Garland Science
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Binding: Hardcover

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Apoptosis is an essential process in embryonic development and tissue homeostasis, particularly in the prevention of disease. Written from a genetic viewpoint, Genetics of Apoptosis first describes the molecular and cell biology of apoptosis, then examines the process in more detail in several model systems. This volume brings together contributions from internationally renowned authors, and will be a valuable reference to all researchers studying apoptosis.

Genomic Instability and Immortality in Cancer (Pezcoller Foundation Symposia)

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Genomic Instability and Immortality in Cancer (Pezcoller Foundation Symposia)

Manufacturer: Springer
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