By William R. Clark
Why can we age? Is getting older inevitable? Will advances in scientific wisdom let us expand the human lifespan past its current limits? simply because getting old has lengthy been the only irreducible truth of human lifestyles, those interesting 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 not easy the idea that human lifespans are past our keep watch over. With such discoveries in brain, famous telephone biologist William R. Clark essentially and elegantly describes how senescence starts off on the point of person cells and the way mobile replication might be certain up with getting older of the total 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 sickness, and the insights received via learning human genetic disorders--such as Werner's syndrome--that mimic the indications of getting older. Clark additionally explains how relief in caloric consumption may very well aid elevate lifespan, and the way the harmful results of oxidative components within the physique could be restricted by way of the intake of antioxidants present in vegetables and fruit. In a last bankruptcy, Clark considers the social and financial elements of residing longer, the results of gene treatment on senescence, and what we'd know about getting older from experiments in cloning. it is a hugely readable, provocative account of a few of the main far-reaching and arguable questions we're more likely to ask within the subsequent century.
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Additional info for A Means to an End - The Biological Basis of Aging and Death
T h e intracellular events that follow receipt of an appropriate "death signal," whatever its origin, are extraordinarily complex and not yet fully understood. Sometimes the response is to commit suicide; sometimes the response (particularly for cells that are rapidly dividing) may simply be to shunt into a state of advanced senescence where they may remain for a long time. We do not yet understand how the choice between these two fates is made, or how or when the newly senescent cells will die.
Very recently it was discovered that the death of the macronucleus in paramecia that have just had sex is essentially identical to the destruction of nuclei in mammalian cells undergoing apoptosis. T h e D N A is fragmented into millions of useless pieces. T h e apoptotic death of the macronucleus in early organisms such as paramecia likely represents the evolutionary beginnings of apoptotic cell death in eukaryotes. Apoptosis of the macronucleus in connection with sexual rejuvenation obviously does not lead to death of the cell, but as we will see in a moment, when carried forward into multicellular animals that is precisely what apoptosis does.
Mouse or rat embryo fibroblasts, for example, divide only about a dozen times; humans, as we have noted, about fifty; and the Galapagos turtle, about 120 times. T h i s is one of the strongest arguments that replicative senescence is in some way tied into the normal aging process. 36 THE NATURE OF CELLULAR S E N E S C E N C E AND DEATH W h a t happens to fibroblasts at the end of their "fife" in vitro is really not known. Despite a few claims to the contrary, there is ample evidence they do not die, at least not as an immediate consequence of the loss of the ability to divide.
A Means to an End - The Biological Basis of Aging and Death by William R. Clark