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In biology senescence is the state or process of aging. For the social, cultural, and economic aspects see ageing. The word senescence is derived from the Latin word senex, meaning "old man" or "old age."

Cellular senescence is a phenomena where isolated cells demonstrate a limited ability to divide in culture. Organismal senescence is 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 organisms. 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.

Theories of aging

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 vary 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.

Evolutionary theories

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 negative 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.

An alternative view of looking at this question is: why do humans live so long? No other primate has such an extended post-reproductive phase of life. The "grandmothering theory" of evolution holds that because humans can teach their young, there was an evolutionary advantage for groups of humans who had a few older survivors to teach and care for the young. There is no particular evidence for this theory.

Gene regulation

The first genetic component of aging was first identified in the budding yeast Saccharomyces cerevisiae. Replicative yeast cell aging is defined as the number of cell division (daughter cells) that can be produced by any given mother cell. Calorie restriction in yeast results in lifespan extension (each mother cell can produce more daughter cells). The gene Sir2 was identified as a gene required for lifespan extension by calorie restriction, and yeast cells without sir2 have a decreased lifespan. Sir2 is a NAD+-dependent histone deacetylase, and is required for genomic silencing at three loci: the yeast mating loci, the telomeres and the ribosomal DNA (rDNA). Yeast replicative aging is caused by homolgous recombination between rDNA repeats; excision of rDNA repeats results in the formation of extrachromosomal rDNA circles (ERCs). These ERCs replicate and preferentially segregate to the mother cell during cell division, and are believed to result in cellular senescence by titrating away essential nuclear factors.

Lately research on a worm called Caenorhabditis elegans has 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.

Cellular senescence

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.

Chemical damage

It is also suggested that damage to long-lived biopolymers, e.g., structural proteins and DNA, caused by ubiquitous chemical agents in the body, such as oxygen and sugars, are in part responsible for aging. The damage can include breakage of biopolymer chains, cross-linking of biopolymers, or chemical attachment of unnatural subtituents (haptens) to biopolymers.

Oxygen spontaneously generates low levels of reactive oxygen species such as singlet oxygen, peroxides and superoxide ion, which can in turn generate free radicals which can damage structural proteins and DNA. Certain metal ions found in the body, such as copper and iron, may participate in the process. (In Wilson's disease, a hereditary defect which causes the body to retain copper, some of the symptoms resemble accelerated senescence.) These processes are termed oxidant damage and are the target of the currently popular nutritional antioxidants.

Sugars such as glucose and fructose can react with certain amino acids such as lysine and arginine and certain DNA bases such as guanine to produce sugar adducts, in a process called glycation. These adducts can further rearrange to form reactive species which can then cross-link the structural proteins or DNA to similar biopolymers or other biomolecules such as non-structural proteins. People with diabetes, who have elevated blood sugar, develop senescence-associated disorders much earlier than the general population, but can delay such disorders by rigorous control of their blood sugar levels. There is evidence that sugar damage is linked to oxidant damage in a process termed glycoxidation.

Chemical damage to DNA can lead to mutations (see above). Chemical damage to structural proteins can lead to loss of function; for example, damage to collagen of blood vessel walls can lead to vessel-wall stiffness and thus hypertension, and vessel wall thickening and reactive tissue formation (atherosclerosis); similar processes in the kidney can lead to renal failure.

Reliability theory

Suggests that biological systems start their adult life with a high load of initial damage.

Neuro-endocrine-immuno theories

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, Biogerontology, Rejuvenation and Brain Aging.

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