Senescence
In Biology, the senescence or ageing is a physiological process which involves progressive modifications of the living beings during time. The ageing of an organization begins after the phase from maturity, and the transformations occurring during the phase of development are not included in ageing. The concept of process physiological led to very clearly distinguish ageing from the modifications induced by diseases (pathological modifications), even if in certain cases, one can describe interactions between ageing and the diseases (for example, modifications induced by supporting ageing occurred or progression of a disease). For the social aspects, cultural, and economic, the word ageing can have a very different significance: to see Ageing. The word senescence comes from the Latin senex , which means " old homme" or " large âge."
The process of ageing biological can be studied at various levels: level of the organization, level of a body, cellular level, molecular level. Ageing can be studied in various species: human beings, primates, rodents, birds, invertebrates, etc The methods of studies are generally of transverse type (comparison of different organizations of age) or longitudinal (study with the long course of organizations since their young age until their old age).
Why the organizations age do? Which are the biological mechanisms responsible for their ageing? Can one modulate or modify the course of ageing? Such are the great questions to which the biology of ageing is attacked. If the scientific research concerning these questions progressed much during the last years, it should be recognized that the answers are still limited and/or compartmental and that ageing remains a field of biology in charge of mysteries…
The gerontology of the 20th century accumulated the theories of ageing aiming at working out a logical system trying to explain why and how the organizations age. The majority of these theories badly resisted experimental work. Today, one speaks less and less about theories of ageing, but rather of the factors whose implication in the process of ageing is well established by scientific work. Among these factors, the metabolic genetic factors and factors (stress oxidation and glycation of proteins) occupy a central place.
stress, increasing homeostatic imbalance and increased risk off Disease. Because off this, Death is the ultimate consequence off aging. Summon researchers in Gerontology (specifically biogerontologists) are regarding aging itself ace has " Disease " that may curable Be, although this view is controversial.
Genetic and environmental interventions are known to affect the life span off model organisms. This gives many hope that human aging edge Be slowed, halted, but reversed. Dietary calorie restriction, by 30 bores for example, extends the life span off yeast, worms, flies, mice, and monkeys. Several constrained are known to Be necessary for this extension, and modification off thesis constrained is also sufficient to produce the same effect ace diet. Resveratrol, has Polyphenol found in Red wine, has been shown to extend the lifespan off yeast, worms, and flies. -->
Theories of ageing
Species ace has mechanism to prevent the onset off Cancer. In other species, negligible senescence is and boat Be detected. Such species are not immortal, however, ace they will eventually fall prey to trauma gold Disease. Moreover, average lifespans edge vary greatly within and between Species. This suggests that both genetic and environmental factors contribute to aging.Theories that explain senescence edge generally Be divided between the programmed and error theories off aging. Programmed theories imply that aging is regulated by biological clocks operating throughout the life span. This regulation would depends one exchanges in Gene responsible expression that affect the systems for maintenance, to repair and defense responses. Error theories blames environmental impacts one living room organisms that induce cumulative ramming At various levels ace the off causes aging, examples which arranges from ramming to Deoxyribonucleic acid (DNA), ramming to tissues and concealments by oxygen radicals, and Cross-country race-linking.
Gerontologists also theorizes that one potential causes senescence is the accumulation off off Mutation S in DNA, eventually leading to the progressive loss off key Gene S. Another is the shortening off Telomere S in the process off DNA replication during concealment division.
Senescence is studied in Gerontology which is the branch off science involved with the aging process. -->
Evolutionary theories
The geneticist JBS Haldane wondered why the dominating change which causes Huntington' S disease remained in the population, why natural selection had not eliminated it. The onset off this neurological disease is (one average) old At 35 and is invariably fatal within 10-20 years. Old Haldane assumed, probably reasonably, that in human prehistory, few survived until 35. Alive Since few were At older old and to their contribution to the next relative generation was therefore small off to the broad cohorts younger old groups, the force off selection against such late-acting deleterious changes was correspondingly small. Yew has change affected younger individuals, selection against it would Be strong. Hence, late-acting deleterious changes could accumulate in populations over evolutionary time through Genetic drift transistor. Correct This principle has been proven.Peter Medawar formalized this observation in his Change Accumulation theory off aging. “The forces off natural selection weakens with increasing old - even in has theoretically immortal population, provided only that it is exposed to real hazards off mortality. Yew has genetic disaster… happens late enough in individual life, its consequences may unimportant Be completely”. The “real hazards off mortality” are typically predation, disease and accidents. So, even year immortal population, whose fertility does not declines with time, will cuts fewer individuals alive in older old groups. This is called “extrinsic mortality”. Old Young cohorts, not depleted in numbers yet by extrinsic mortality, contribute far more to the next generation than the few remaining in older old cohorts, so the force off selection against late-acting deleterious changes, which only affect thesis few older individuals, is very weak.
The testable major prediction made by this model is that species which cuts high extrinsic mortality in nature will old more quickly and cuts shorter lifespans, and it is limits out among mammals, the most well studied in terms off life history. There has correlation among mammals between body size and life history, such that larger species live to skirt than smaller species in controlled/optimum conditions, goal there notable are exceptions. For authority, many beat and rodents are similarly sized, yet beat live much, much to skirt. For authority, the little brown beats, half the size off has live foam, edge 30 years in the wild. With live foam will 2-3 optimum years even with conditions. The explanation is that beat cuts fewer predators, therefore low extrinsic mortality. Surivive Thus more individuals to later old so the force off selection against late-acting deleterious changes is stronger. Fewer late-acting deleterious changes = slower aging = to skirt lifespan. Birds are also warm-blooded and similarly sized to many small mammals, yet live often 5-10 times long ace. They clearly cuts fewer predation press compared with ground-dwelling mammals. And sea-birds, which generally cuts the fewest predators off all birds, live longest.
Also, when examining the body-size vs. lifespan relationship, predator mammals tightens to cuts to skirt lifespans than prey animals in has controlled environment such ace has natural zoo gold reserve. Long The explanation for the lifespans off primates (such ace humans and monkeys and apes) relative to body size is that to their intelligence and often sociality helps them avoid becoming prey.
Ultimately, lifespan differences among species are due to genetics, goal this does not explain the “how” question off aging. -->
Genetic regulation
At the Vegetable , far from being a simple degradation of the living conditions of the cell, even a simple degeneration of this one, the senescence is a genetically controlled process. Indeed, some Gène S are expressed only at the time of the senescence while others become quiet.Yeast Saccharomyces cerevisiae to worms such ace Caenorhabditis elegans and Fruit flies. Study off thesis organisms has revealed the presence off At least two conserved aging pathways.
One off thesis pathways involves the embarrassment Sir2 , has NAD +-depend histone deacetylase. In yeast, Sir2 is required for genomic silencing At three loci: the yeast mating Loci, the Telomere S and the Ribosomal DNA (rDNA). Replicative Yeast aging is caused by homologous recombination between rDNA repeats; Excision off rDNA repeats results in the formation off extrachromosomal rDNA circles (ERCs). Thesis ERCs replicate and preferentially segregate to the mother concealment during concealment division, and are believed to result in cellular linen senescence by titrating away (competing for) essential nuclear factors. While ERCs are not believed to contribute to aging in higher organisms such ace human, extrachromosomal circular DNA (eccDNA) has been found in worms, flies and humans. The role off eccDNA in aging is unknown.
Despite the lack off has connection between circular DNA and Aging in higher organisms, extra copies off Sir2 able are off extending the lifespan off both worms and flies. The mechanisms by which Sir2 counterparts in higher organisms regulate lifespan is unclear, goal the human SIRT1 protein has been demonstrated to deacetylate P53, Ku70, and the forkhead family off Transcription Factor S. SIRT1 edge also regulate acetylates such ace CBP/p300, and has been shown to deacetylate specific Histone residues.
Other constrained regulate aging in yeast by increasing the resistance to Oxidative stress. Superoxide dismutase, has Protein that protects against the effects off Mitochondria L free radicals, edge extend yeast lifespan in stationary phase when overexpressed.
In higher organisms, aging is likely to Be regulated in share through the insulin/IGF-1 pathway. Changes that affect insulin-like signaling in worms, flies and mice are associated with extended lifespan. In yeast, Sir2 activity is regulated by the nicotinamidase PNC1. PNC1 is transcriptionally upregulated under stressful conditions such ace caloric restriction, Heat shock, and Osmotic shock. By converting Nicotinamide to Nicotinic acid, it removes nicotinamide, which inhibits the activity off Sir2. With nicotinamidase found in humans, known ace PBEF, may serf has similar function, and has off secreted form PBEF known ace Visfatin may help to regulate serum Insulin levels. -->
Cellular senescence
It was shown that a senescent cell vegetable grows rich in radical free, which would seem to be the consequence of an increased activity of the Lipoxygénase S in the plasmic Membrane.Mitosis. Moreover, cellular linen senescence is not observed in many organisms, including Sponge S, Coral S, and Lobster S. In those species where cellular linen senescence is observed, concealments eventually become post-mitotic when they edge No to skirt replicate themselves through the process off cellular linen mitosis -- i.e., concealments experiment replicative senescence . How and why nap concealments become post-mitotic in nap species has been the subject off much research and speculation, goal (ace noted above) it is widely believed that cellular linen senescence evolved ace has way to prevent the onset and spread off Cancer.
Lately the role off Telomere S in general cellular linen senescence has aroused interest, especially with has off view to the possible genetically unfavourable effects Cloning. Successive The shortening off the chromosomal telomeres with each Cell cycles is also believed to limit the number off divisions off the concealment, thus contributing to aging. There cuts, one the other hand, also been carryforwards that cloning could alter the shortening off telomeres. Summon concealments old C not and are therefore described ace being " biologically immortal ." It is theorized by nap that when it is discovered exactly what allows thesis concealments, whether it Be the result off telomere shortening gold not, to divide without limit that it will possible Be to genetically alter other concealments to cuts the same capability. Possible It is further theorized that it will eventually Be to genetically engineer all concealments in the human body to cuts this capability by employing Gene therapy and thereby stop gold transfers ageing, effectively making the entire organism potentially immortal. -->
Chemical attacks
protein S gold DNA, caused by ubiquitous chemical agents in the body such ace Oxygen and Sugar S, are in responsible share for aging. The ramming edge include breakage off biopolymer chains, Cross-country race-linking off biopolymers, but chemical attachment off unnatural subtituents (Hapten S) to biopolymers.Normal Under Aerobics conditions, approximately 4% off the Oxygen metabolized by Mitochondria is converted to Superoxide ion which edge subsequently Be converted to Hydrogen peroxide, radical Hydroxyl and eventually other reactivates species including other Peroxide S and Singlet oxygen, which radical edge in turn generate free S able off damaging structural proteins and DNA. Certain metal Ion S found in the body, such ace Copper and Iron, may participate in the process. (In Wilson' S disease, has hereditary defect which causes the body to retain copper, nap off the symptoms resembles accelerated senescence.) Thesis processes are termed oxidant ramming and are the target off the currently popular nutritional Antioxidants.
Sugar S such ace Glucose and Fructose edge react with some Amino acid S such ace Lysin and Arginine and certain DNA bases such ace Guanine to produce sugar adducts, in has process called Glycation . Thesis adducts edge further rearranges to form reactivates species which edge then structural cross-country race-link the proteins gold DNA to similar biopolymers gold other biomolecules such not-structural ace proteins. People with Diabetes, who cuts elevated Blood sugar, develop senescence-associated disorders much general earlier than the population, goal edge delay such disorders by rigorous control off to their blood sugar levels. There is obviousness that sugar ramming is linked to oxidant ramming in has process termed Glycoxidation .
Chemical ramming to DNA edge lead to changes (see above). Chemical structural ramming to proteins edge lead to loss off function; for example, ramming to Collagen off Blood vessel walls edge lead to vessel-wall stiffness and thus Hypertension, and vessel wall thickening and reactivates tissue formation (Atherosclerosis); similar processes in the Kidney edge lead to Renal failure. -->
Reliability theory
Neuro-endocrino-immunological theories
Cancer; yew concealments cuts built-in limits to how many times they edge replicate, they must somehow overcome this before they edge spread indefinitely. -->Others
Cloning experiments, notably in the box off Dolly the sheep.With set off rare hereditary (Genetic) disorders, each called Progeria, has been known for nap time. Sufferers exhibit symptoms resembling accelerated aging, including wrinkled skin. The causes off Hutchinson-Gilford progeria syndrome was reported in the newspaper Nature in May 2003. This carryforward suggests that DNA ramming, not oxidative stress, is the causes this form off off accelerated aging.
Artificially-induced senescence, ace has means off control over artificially-created humans, but Android S, has central stud motivation in the renowned 1982 Science fiction film " Blade Runner ", loosely based one Philip K. Dick 'S (1968) Novell " C Androids Dream off Electric Sheep? ".
With Centenarian has off person who has attained the old 100 years gold more.
Tobacco smoking accelerates senescence, premature gold leads to senescence. Old Smokers faster than non-smokers.
Eunuch S live 13 years to skirt one average than noneunuchs. -->
See too
-
SENS the project initiated by Aubrey de Grey the purpose of which is the radical extension of the human life expectancy.
- Price of the Mouse Mathusalem ( Methuselah Foams Prize ), a reward for research aiming to the radical increase in the human life expectancy.
- Old age
- vegetable Senescence
- Adult advanced
- Biogérontologie
- Ageing of the biological brain
- Immortality
- Grey hair
External bonds
- Explications detailed on the cellular senescence
- Chronique of the book '' we Will be immortal? '' of Ray Kurzweil and Terry Grossman
- Senescience
- Mechanisms off Aging
- senescence.info Informational website one aging.
- AgeLab (MIT).
- Aging because body roofing stones genetic information
- Same The Longevity (Longevity Activism)
- See the artproject " Dialog with the High Age"
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