Cellular senescence refers to a phenomena where isolated cells demonstrate a limited ability to divide in culture. Organismal senescence refers to the aging of organisms.
Organismal aging is generally characterized by the declining ability to respond to stress, increasing homeostatic imbalance and increased risk of disease. Because of this, death is the ultimate consequence of aging.
Genetic and environmental interventions are known to affect the life span of model organsims. This gives many hope that human aging can be slowed or changed. Dietary calorie restriction, by 30 percent for example, extends the life span of yeast, worms, flies, mice, and monkeys. Several genes are known to be necessary for this extension, and modification of these genes is also sufficient to produce the same effect as diet.
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2 Evolutionary theories 3 Gene regulation 4 Cellular senescence 5 Free radicals 6 Reliability theory 7 Neuro-endocrine-immuno theories 8 Misc |
The process of senescence is complex, and may derive from a variety of different mechanisms and exist for a variety of different reasons. Senescence is a universal biological phenomea, at least amongst eukaryotic organisms. Yet the average lifespan within and between species can very greatly. This suggests that both genetic and environmental factors contribute to aging.
Theories that explain senescence can generally be divided between the programmed and error theories of aging. Programmed theories imply that aging is regulated by biological clocks operating throughout the life span. This regulation would depend on changes in gene expression that affect the systems responsible for maintenance, repair and defense responses. Error theories blame environmental insults to living organisms that induce cummulative damage at various levels as the cause of aging (e.g., DNA damage, oxygen radicals, cross-linking).
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 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.
One possible mechanism may be "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 deleterious effect 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 gene doesn't have a negatgive effect until after the individual has reproduced, the gene may escape natural selection altogether, because when selection starts to affect the gene, it has already propagated to the next generation.
Lately research on a worm called Caenorhabditis elegans have demonstrated that aging is in part regulated by genes. The worm's short life span can be increased by more than 200 percent through genetic engineering. For example, mutations that affect insulin-like signaling in worms, flies and mice are associated with extended lifespan.
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 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 alter the shortening of telomeres.
It is also suggested that damage caused by free radicals in the body are in part responsible for aging.
Suggests that paradoxical conjecture that biological systems start their adult life with a high load of initial damage.
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.
Recently, early senescence has appeared as a possible unintended outcome of early cloning experiments, notably in the case of Dolly the sheep.
A set of rare hereditary (genetic) disorders, each called progeria, has been known for some time. Sufferers exhibit symptoms resembling accelerated aging, including wrinkled skin. The cause of Hutchinson–Gilford progeria syndrome was reported in the journal Nature in May 2003. This report suggests that DNA damage, not oxidative stress, is the cause of this form of accelerated aging.
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".
Centenarian is a person who has attained the age of 100 years or more.
Smoking cigarettes accelerates senescence, or leads to premature senescence. Smokers age faster than non-smokers.
See also Advanced adult, Cigarette, and Rejuvenation.Theories of aging
Evolutionary theories
Gene regulation
Cellular senescence
Free radicals
Reliability theory
Neuro-endocrine-immuno theories
Misc