Download A Means to an End: The Biological Basis of Aging and Death by William R. Clark PDF

Cell Biology

By William R. Clark

Why will we age? Is getting older inevitable? Will advances in clinical wisdom let us expand the human lifespan past its current limits? simply because growing old has lengthy been the single irreducible truth of human lifestyles, those exciting questions come up extra frequently within the context of technology fiction than technological know-how truth. yet fresh discoveries within the fields of mobile biology and molecular genetics are heavily difficult the idea that human lifespans are past our keep an eye on. With such discoveries in brain, famous cellphone biologist William R. Clark sincerely and elegantly describes how senescence starts on the point of person cells and the way mobile replication can be sure up with getting older of the complete organism. He explores the evolutionary beginning and serve as of getting older, the mobile connections among getting older and melanoma, the parallels among mobile senescence and Alzheimer's disorder, 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 elevate lifespan, and the way the damaging results of oxidative parts within the physique can be constrained through the intake of antioxidants present in vegetables and fruit. In a last bankruptcy, Clark considers the social and financial points of residing longer, the results of gene treatment on senescence, and what we would 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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Studies of this type began shortly after the turn of the present century. Limiting food intake in a wide range of laboratory organisms—from single-cell organisms through rats and mice—was found to increase maximal lifespan, in some cases up to double the normal maximum lifespan. In warm-blooded animals, it is the only known way to modulate maximum lifespan. The dietary restriction effect was most pronounced if restriction was initiated prior to the reproductive period, although restriction of caloric intake in older animals can also be effective in prolonging lifespan.

Unravelling how this death program works in cells induced to undergo apoptosis is one of the most active areas of current research in cell biology. The signal to commit suicide can also come from within the cell itself, for example, if cellular machinery set up for that purpose detects excessive DNA damage within the cell's nucleus, or determines that the cell has been invaded by a virus or has become cancerous. The intracellular events that follow receipt of an appropriate "death signal," whatever its origin, are extraordinarily complex and not yet fully understood.

So senescence and compulsory death did appear at a specific point in evolution, and they did have to be selected and fixed as stable traits in those species in which they evolved. There was no other choice for paramecia or for any of the other protists in which it occurs, once sex was used to create new genetic combinations. And in a very real sense, 3O 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 the death of the macronucleus in paramecia predicts our own corporeal deaths.

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