A Means to an End: The Biological Basis of Aging and Death
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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A means to an end: the biological basis of aging and deathUser Review - Not Available - Book Verdict
As in his previous books, Clark (immunology, emeritus, UCLA; The New Healers: Molecular Medicine in the Twenty-First Century, LJ 12/97) does not hesitate to introduce the lay reader to complex ... Read full review
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ability accidental death active aging process alleles Alzheimer's disease antioxidants apoptosis average lifespan biological body brain caloric restriction calorically restricted diet cancer cardiovascular cause cell cycle cell death cell division cellular senescence changes chromosome cyclin decade defect dietary divide DNA damage DNA repair effect elegans embryonic eukaryotes evolution evolutionary factor females fibroblasts fully fed function genetic genome germ cells growth signals helicase HGPS human aging human lifespan important increase individuals involved large numbers live longer macronucleus major maximal maximum lifespan mechanisms metabolic mice molecular molecules multicellular mutations neuritic plaques neurons normal aging number of cell offspring oncogenes onset organism oxidative damage oxygen radicals paramecia patients percent phenotypes population produced progerias prokaryotes proteins rats replicative senescence reproductive maturity result role senescence and death simply skin species studies syndrome telomerase telomeres tion tissues tumor tumor suppressor genes vitamin vitro Werner's syndrome yeast