Redirected from Aging
The process of senescence is complex, and may derive from a variety of different mechanisms and exist for a variety of different reasons.
One view is that it is due to a particular DNA programming that has the sole purpose to "clean" Earth from old genes and assure offspring better living conditions through benign mutations. Lately research on a worm called Caenorhabditis elegans showed the ability to increase its short life span by about 40% thanks to mutations artificially induced through genetic engineering. It is also suggested that reactions caused by free radicals in the body are responsible for aging.
One potential cause of senescence is the accumulation of mutations in DNA, eventually leading to the progressive loss of key genes. Another is the shortening of telomeres in the process of DNA replication during cell division.
One possible mechanism may be special "senescence genes". Genes which have a deleterious effect on individual's fitness are selected against by natural selection. Mutations in these genes which postpone the expression of the gene to a later time in individual's life history[?] reduce the effect of natural selection to the gene, because the selection has less time to act on it. If the expression doesn't take place until the individual has reproduced, the gene escapes natural selection altogether, because when selection starts to affect the gene, it has already propagated to the next generation.
Senescence may also simply be a result of wear and tear overwhelming repair mechanisms. It is also possible that senescence is a mechanism to control the development and spread of cancer; if cells have built-in limits to how many times they can replicate, they must somehow overcome this before they can spread indefinitely.
Lately the role of telomeres has aroused general interest, especially with a view to the possible genetically adverse effects of cloning. The successive shortening of the chromosomal telomeres with each natural cell cycle is also believed to influence the vitality of the cell, thus contributing to aging. There have, on the other hand, also been reports that cloning could in fact help suppress or even reverse the shortening of telomeres.
Artificially-induced senescence, as a means of control over artificially-created humans, or androids, is a central plot motivation in the renowned 1982 science fiction film "Blade Runner", loosely based on Philip K. Dick's (1968) novel "Do Androids Dream of Electric Sheep?".
See also Advanced adult.