AGING : the chronic-degenerative disease with the longest incubation time; the gradual deterioration in the structure of any organism that occur with the passage of time, that do not result from disease or other gross accidents, and that eventually lead to the increased probability of death as the individual grows olderref Epidemiology : maximum age : The duration of life seems to be inversely related to proliferation rate. The limiting factor are perennial tissues, where apoptosis are only partly compensated by hypertrophy of remaining cells.
Do all species undergo senescence ? An increase in the age-specific death rate with increasing adult calendar age is one criterion that has been used and the other is decreasing fecundity with increasing calendar age. However, so few species have been assessed for these criteria that an answer to the question of universality cannot be given with anything near certainty. Indeed, rock fish, sturgeons, and carp appear to live to advanced ages without evidence of an increase in age-specific death rates or a decrease in fecundity. However, it is quite possible that these species have not been studied carefully enough to detect such changes if, in these species, they progress at an extraordinarily slow rate. Biologists have long believed that senescence occurs in those species with a germ line that is separate from the soma and that it is only the soma that undergoes senescence : however, recent findings have shown that senescence can occur in organisms that do not have a germ line separate from the soma, such as some species of yeast. Senescence occurs in most, if not all, species that undergo sexual reproduction, including yeasts.
Aetiology : the second law of thermodynamics states that with the passage of time, there is an increase in entropy : living organisms are not closed systems, but rather they are thermodynamically open systems. Specifically, living organisms utilize the matter and energy in food (and light, in the case of photosynthetic organisms) to counter entropy. The maintenance of this complex adult organism would appear to be a far less formidable challenge than its development. Yet even when the supply of external matter and energy is unlimited, it appears that most, if not all, species of complex organisms are not able to prevent deterioration of their structure and function during the adult period of life. Aging is clearly not a thermodynamic inevitability, and yet it occurs widely in nature. Therefore, it must be concluded that the ability to utilize external matter and energy to maintain complex function and structure is progressively lost by most animals and plants with advancing adult calendar age. Why don't evolutionary forces eliminate a process, such as senescence, that is so detrimental to the ability of individual organism to maintain itself and generate progeny ? The extent of the increase in risk of mortality is assessed by determining the increase in age-specific death rate with increasing calendar age = the fraction of the population of a given age that dies during a time interval. The increase in the age-specific death rate with advancing calendar age is an index of increasing vulnerability due to senescence. A cohort is a group of individuals that share a statistical characteristic. In the case of the animals in gerontologic laboratory studies, a cohort usually refers to individuals born during a particular period of time.
In addition to an increasing risk of mortality, many anatomical and physiological changes occur (mostly deteriorative) : the extent to which such changes are the result or the cause of the age-associated increase in vulnerability or organisms is not known and undoubtedly varies with the particular anatomical or physiological change. There is a great deal of individual variation in the occurrence and the magnitude of age changes in anatomical structures and physiological systems. Most elderly people do exhibit substantial deterioration in many physiological systems, reducing ability to cope with challenges and functional capacity. Age-associated diseases are those that occur only at advanced ages or are more prevalent in the old : cancers primarily occur after 2 years of age in rats, while in humans they occur mostly after 50 years of age. Moreover, each species has a set of age-associated diseases that differ from those found in other species. In humans, the increases in morbidity (a disease state) and mortality due to coronary heart diseases, stroke, type II DM, osteoporosis, Alzheimer's disease, Parkinson's disease, and prostatic cancer relate to calendar age in a fashion similar to that of the increase in age-specific death rate. Although multiple sclerosis, amyotrophic lateral sclerosis, gout, peptic ulcer, and most cancers are aso age-associated, their occurrence does not parallel the increase in age-specific death rate.
Pathogenesis : the general pattern of aginig appears to be similar for most mammalian species. In no case has supporting evidence been sufficient to justify using the word "theory"; "hypothesis" would be he more appropriate term. Since senescence probably stems from many different proximate mechanisms and their interactions, strong evidence in support of a single mechanism seem highly unlikely. Most of the poposed mechanisms are based on a particular characteristic of the aging phenotype : unfortunately, it is difficult to know whether such a characteristic plays a causal role in senescence or is rather the result of senescenceref1, ref2, ref3, ref4, ref5. Somatic cloning bypasses the selection mechanisms acting on gametes => high mortality and low life expectancy in newborns. The disposable soma theory of aging proposed by Thomas Krkwood postulates that the besic function of all organisms is to utilize free energy in the enviroment to produce progeny : to do so requires that a portion of the energy be used for the maintenance of the organism. The force of selection acts to apportion the use of energy between reproduction and somatic maintenance in a fashion that tends to maximize evolutionary fitness : less energy is used for somatic maintenance than is required for indefinite survival - and thus the occurrence of senescence The proximate mechanism of aging should be divided into 2 classes : the "private" category refers to mechanisms that are idiosyncratic to certain lineages, populations, or species, while the "public" category refers to mechanisms generally operational among a diverse group of species. This classification addresses the apparent paradox that while senescence exhibits general similarities among a broad range of different species, there are many specific differences in the aging phenotype of various species and, indeed, among members of the same species. Mutations with deleterious late-life actions will most likely be in the private category, based on the fact that such mutations are neutral in regard to natural selection, neither favoring nor disfavoring evolutionary fitness in young adults. Since genetic drift determines their presence, their occurrence would be expected to vary among lineages. Examples include the ones that cuase Huntington's disease and the e4-allele of apolipoprotein E locus (found in approximately 15% of European adults) which increases the risk of coronary heart disease and late-onset Alzherimer's disease. This view should be broadened to include all traits that have a detrimental action expressed at advanced ages, rather than being restricted solely to well-defined mutations. For example, essentially all humans show a progressive bone los with advancing age, which appears to be a species genetic trait (and thus a private mechanism) since it does not occur in most mammalian species. Second, it seems likely that antagonistic pleiotropy can also be involved in "private" mechanisms. Indeed, the male sex hormone, so importantly involved in young men generating progeny, has been implicated inn the late-life occurrence of prostate cancer and coronary heart disease, a clear example of antagonistic pleiotropy. Public mechanisms are most likely to be associated with antagonistic pleiotropic genes as there are a relatively small number of processes in which functions are beneficial in early life and harmful in late life, and such genes will be maintained by strong selective forces andtherefore are likely to spread widely among individuals and species. Such genes have yet to be clearly identified : antagonistic pleiotropy, in so far as it occurs, is likely to primarily underlie private mechanisms of senescence. "Public" mechanisms are likely to be in the domain of the disposable soma theory : accumulation of damage occurs in all organisms that undergo senescence. In the classical view, senescence is deemed an entirely intrinsic process; and second, age-associated iseases are not considered a part of "normal" aging. If senescence, results from the long-term accumulation of unrepaired damage, it is immaterial wheteher the damage is caused by intrinsic processes or by extrinsic (environmental) factors. Extrinsic agents cause damage by interacting with biological materials and activities; and in this sense, all damage is intrinsic. Environmental factors are often the most important factors underlying senescence. The very old invidiual, free of discernible disease, is nevertheless recognized as frail; arbitrariy, that fraility is referred to as physiological deterioration, and thus, according to the classical view, the person has undergone "normal" aging, i.e., aging in the absence of a disease. The elderly person whose physiological deterioration is recognized by a physician as due to an age-associated disease and the elderly person whose physiological deterioration is recognized only as old age are both experiencing the effects of senescence. Senescent deterioration in humans is primarily a function of lifestyle. "Private" mechanisms play a dominant role in human aging; however, "public" mechanisms, such as oxidative stress, may well be involved in these "private" mechanisms. Each spescies must be assessed separately because it is clear from the available information that the aging of each species is, in some way, unique to that speciesref1, ref2, ref3.
Symptoms & signs : although some of the age changes in anatomical and physiological characteristics may be a cause of senescence, most are probably the result of it. Some phenotypic changes may have little to do with organismic senescence. For example, there is no evidence that graying of the hari increases a person's vulnerability or decreases the ability to function. Thus, although associated with advancing calendar age, graying of hair probably does not belong in the category of senescence. A fingerprint of gene activity could reveal the true 'youthfulness' of our kidneys, hearts and muscle, regardless of our biological age. The technique might one day be used to find healthy organs for transplants or to warn us of impending disease. It's hard to tell, particularly on a cellular level, whether a young and healthy body conceals a withering heart — or conversely, whether an old man has a vigorous ticker like that of a younger man. Activity of a set of genes reveals how well organs are operating, regardless of their owner's actual age. The team analysed the activity of thousands of genes in 81 muscle samples from people aged between 16 and 89. They pulled out a set of 250 genes whose activity goes markedly up or down with age. When they compared the activity of these genes with the muscle fitness of individuals, measured by the size of their muscle fibers, they found that the genetic profile, rather than a person's age in years, was a more accurate indicator of fitness. The speed with which our cells and bodies deteriorate is determined partly by the genes we inherit from our parents and partly by the ravages of living. These factors can change the rate at which certain genes manufacture proteins, and other aspects of the cell's machinery. Some studies, for example, have shown that telomeres decay over time and do so faster in those who indulge in unhealthy activities such as smoking. One 64-year-old man had a pattern of gene activity more like that of a younger person : indeed, under the microscope, his muscle appeared young; it contained bigger 'fast twitch' fibers that are good for sprinting and more prevalent in young muscleref. In an earlier study, the same group detected a 78-year-old woman with a kidney more like that of a centenarian, according to her genetic profile and an inspection of the tissue under the microscoperef. The researchers found that aging affects some of the same genes across many different tissue types and in many different animals. One group of genes, which is involved in generating energy in the cell's mitochondria, quiet down with age in human muscle, kidney and brain tissue, and also in aging mice and flies, even though these animals have very different lifespans. It may be that this pathway is a weak spot in the cell that is particularly vulnerable to aging. Such techniques could one day be used to identify donor organs that are normally ruled out because of the donor's age but may actually be in good working order. In future, a routine blood test at the doctor's office could also reveal the true working condition of organs, allowing patients to modify their lifestyle or diet to rejuvenate their bodies. But to do this researchers will need to find a way to gauge the activity of an organ's genes from molecules in the blood rather than from a tissue sample, which is difficult to obtain
Prevention : possible interventions to retard agingref Therapy : gerontotherapeutics / gerontotherapy : therapeutic management of aging persons designed to retard and prevent the development of many of the aspects of senescence. Successful aging is defined in terms of ability of the individual to maintain the following characteristics into advanced ages : low risk of disease and disease-related disability, high mental and physical functioning, and active engagement with life Bibliography : Web resources :
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