By William R. Clark
Why can we age? Is getting older inevitable? Will advances in clinical wisdom let us expand the human lifespan past its current limits? simply because getting older has lengthy been the only irreducible fact of human lifestyles, those exciting questions come up extra frequently within the context of technology fiction than technological know-how truth. yet contemporary discoveries within the fields of telephone biology and molecular genetics are heavily tough the idea that human lifespans are past our keep an eye on. With such discoveries in brain, famous mobilephone biologist William R. Clark truly and elegantly describes how senescence starts on the point of person cells and the way mobile replication might be sure up with getting older of the complete organism. He explores the evolutionary foundation and serve as of getting older, the mobile connections among getting older and melanoma, the parallels among mobile senescence and Alzheimer's affliction, and the insights won via learning human genetic disorders--such as Werner's syndrome--that mimic the indications of getting older. Clark additionally explains how aid in caloric consumption may very well support raise lifespan, and the way the harmful results of oxidative components within the physique might be restricted by way of the intake of antioxidants present in vegatables and fruits. In a last bankruptcy, Clark considers the social and fiscal facets of residing longer, the results of gene treatment on senescence, and what we'd know about getting older from experiments in cloning. this can be a hugely readable, provocative account of a few of the main far-reaching and debatable questions we're prone to ask within the subsequent century.
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Extra info for A Means to an End: The Biological Basis of Aging and Death
We can think of this scheme as one part of the "programmed death" of the organism, but we must define our terms carefully. Clearly there is no defined program, in the sense of a series of steps that are executed in a set sequence, eventually culminating in death of an organism. Rather, a collection of senescence-inducing mechanisms, based on cellular senescence and leading to the eventual extinction of the somatic organism, has become part of the eukaryotic heritage. A very large proportion of these mechanisms were in fact already in place in the earliest single-cell eukaryotic organisms.
One of the potentially most damaging changes that can occur within a cell as it ages is mutation of the DNA. This can be caused by toxic oxidative wastes generated within the cell, or by radiation impinging on those cells that lie close to the surface of the body. Damage to DNA by ultraviolet components of sunlight is a major factor in aging of the skin, and a major cause of skin cancer. Cells are equipped to repair DNA damage, but this ability falls off with age, and the 38 T H E N A T U R E O F C E L L U L A R S E N E S C E N C E A N D DEATH resulting alterations in DNA, including loss of gene function, is thought to be a major cause of senescence in both dividing and nondividing cells.
The contents of the cell spill out, and in many higher animals trigger an inflammatory response that in itself can be damaging to surrounding tissues. In apoptosis, the intracellular architecture is not disturbed, and the cell does not rupture; rather, it fragments into small "apoptotic bodies" that, in multicellular animals, are ingested by neighboring cells. Until the moment of ingestion, organellar function inside these apoptotic bodies seems to go on more or less normally. But perhaps the most interesting feature of apoptosis occurs inside the cell's nucleus.
A Means to an End: The Biological Basis of Aging and Death by William R. Clark