progressive physiological changes in an organism that lead to senescence, or a decline of biological functions and of the organism's ability to adapt to metabolic stress. Many debilitating changes associated with old age in both humans and animals are now attributed to disease processes, such as atherosclerosis or Alzheimer's disease, which occur more frequently with advancing age, rather than to the natural aging process itself. Some deterioration of bodily functions, however, accompanies normal aging. There are many theories about why senescence occurs, most postulating that small alterations in cellular functions accumulate to the point that they impair the function of the organism as a whole. It has been suggested that mutations occur with age in working cells, so that the proteins produced by the cells are no longer capable of normal functions. Insoluble substances called age pigments are also believed to build up in cells over time, eventually interfering with the cells' metabolism, and individual cells eventually wear out, causing breakdowns in organ function. Laboratory experiments have demonstrated that cells from complex organisms go through only a limited number of cell divisions before they die off, supporting the idea that cellular events can produce senescence. On the other hand, the effects of age on the organism as a whole are generally greater than on its component cells. Aging in all organisms appears related to the reproductive cycle. In plants and animals that reproduce once, near the end of the life span, senescence is precipitous once the reproductive act has been completed. In organisms that reproduce several times, senescence is more gradual, beginning during the reproductive phase and continuing until death. A major manifestation of senescence in mammals is the loss of lean body mass, often accompanied by increases in fat and body water. As part of this process, muscle tissue is steadily lost throughout adult life; thus, older individuals are often weaker and less able to exert themselves physically. As lean body mass decreases, the basal metabolic rate (the rate at which the body converts food into energy while at rest) also decreases. Other significant changes take place in the connective tissues. In humans, aging causes a loss of calcium from the bones, increasing the fragility of the skeleton and slowing the rate of healing of fractures; this process, called osteoporosis, is particularly pronounced in women past the age of menopause. All mammals experience a general stiffening of connective tissues with age. Collagen, a fibrous protein found in bones, skin, and tendons, is constantly produced early in life as a soluble molecule that is converted to a sturdier, insoluble form of collagen. As an organism grows older, the production of new collagen ceases, so that connective tissue consists increasingly of the stiffer, insoluble form. This increased stiffness reduces the permeability of connective tissue to nutrients, hormones, and other substances, and contributes to reduced elasticity in the skin, causing wrinkle formation and increased skin fragility in elderly persons. Similar changes occur in elastin, another fibrous protein found in the walls of the blood vessels. Stiffening of the elastin in blood vessels may contribute to high blood pressure by resisting blood flow, increasing the workload on a heart that has already been weakened by the loss of muscle mass. Changes in the nervous system associated with aging chiefly reflect the inability of nerve cells to renew themselves once the animal reaches adulthood. In humans the number of peripheral nerve fibres declines during adult life, and cells from the cerebral cortex may also be lost. The total number of nerve cells, however, is so great that these losses may not have functional effects. Tissues that do retain the ability to renew themselves through most of life begin to lose that ability with age. These tissues contain fewer proliferative cells to replace dying cells, and the rate of cell division in those proliferative cells that remain may be reduced. Effects of this decline include reduced ability to heal wounds, to replenish blood cells lost to injury or disease, and to produce immune cells to combat infection. The declining proliferative capacity of reproductive cells may also end the reproductive life of females (menopause) and reduce the reproductive ability of males. Plants also undergo senescence, exhibiting structural as well as functional deterioration. The characteristics altered by age include: leaf structure (e.g., simple to compound), growth habit (e.g., vining to treelike), stem composition (e.g., soft to woody, thorny to smooth), and bark surface (e.g., smooth to furrowed). The onset of reproductive capability in plants signals a change to the adult life habit; flowers are produced and fruiting occurs, but regenerative capacity (e.g., ability to root from cuttings) declines. progressive physiological changes in an organism that lead to senescence, or a decline of biological functions and of the organism's ability to adapt to metabolic stress. Aging takes place in a cell, an organ, or the total organism with the passage of time. It is a process that goes on over the entire adult life span of any living thing. Gerontology, the study of the aging process, is devoted to the understanding and control of all factors contributing to the finitude of individual life. It is not concerned exclusively with debility, which looms so large in human experience, but deals with a much wider range of phenomena. Every species has a life history in which the individual life span has an appropriate relationship to the reproductive life span and to the mechanism of reproduction and the course of development. How these relationships evolved is as germane to gerontology as it is to evolutionary biology. It is also important to distinguish between the purely physicochemical processes of aging and the accidental organismic processes of disease and injury that lead to death. Gerontology, therefore, can be defined as the science of the finitude of life as expressed in the three aspects of longevity, aging, and death, examined in both evolutionary and individual (ontogenetic) perspective. Longevity is the span of life of an organism. Aging is the sequential or progressive change in an organism that leads to an increased risk of debility, disease, and death; senescence consists of these manifestations of the aging process. The relation of survivorship curves (A) to age-specific mortality rate curves (B). These curves The relation of survivorship curves (A) to age-specific mortality rate curves (B). These curves The viability (survival ability) of a population is characterized in two actuarial functions: the survivorship curve (A in Figure 1) and the age-specific death rate, or Gompertz function (B in Figure 1). The relation of such factors as aging characteristics, constitutional vigour, physical factors, diet, and exposure to disease-causing organisms to the actuarial functions is complex; there is, nevertheless, no substitute for them as measures of the aging process and of the effect of environmental or genetic modifiers. The age-specific mortality rate is the most informative actuarial function for investigations of the aging process. It was first pointed out by an English actuary, Benjamin Gompertz, in 1825 that the mortality rate increases in geometric progressioni.e., by a constant ratio in successive equal age intervals. Hence, a straight line, known as the Gompertz function, results when death rates are plotted on a logarithmic (ratio) scale. The prevalence of many diseases and disabilities rises in the same geometrical manner as does the mortality rate, important exceptions being some infectious diseases and diseases arising from disturbances of the immunological system. Although the life tables of most species are remarkably similar in form, even closely related species can differ markedly in the relative incidence of the major causes of death. George A. Sacher Nathan Wetherill Shock Additional reading General considerations are addressed by John A. Behnke, Caleb B. Finch, and Gairdner B. Moment (eds.), The Biology of Aging (1978), a collection of articles covering many aspects of the subject, including aging in cells and molecules, aging in plants and animals, and evolutionary considerations; Michael R. Rose, Evolutionary Biology of Aging (1991), a provocative treatise that proposes an explanatory theory of aging grounded in evolutionary biology, of value to gerontologists, population geneticists, and other interested readers; Robert R. Kohn, Principles of Mammalian Aging, 2nd ed. (1978), with emphasis on the role of interstitial tissue changes in the aging process; Bernard L. Strehler, Time, Cells, and Aging, 2nd ed. (1977), an examination of cellular and molecular mechanisms and theories of aging; Brian Charlesworth, Evolution in Age-Structured Populations, 2nd ed. (1994), a theoretical consideration of the consequences of age-structure and age-specific differences in reproduction and mortality, which also considers the broader issue of life-history evolution and hence treats senescence as a part of the continuum of development; Caleb E. Finch, Longevity, Senescence, and the Genome (1990), an encyclopaedic treatment of the theories of aging, the statistical methods for evaluating aging, and the full range of empirical methods used to study the aging process for all levels of biological organization, ranging from molecules to populations, with tables and summaries of observed maximum life spans and mortality rates; and Robert E. Ricklefs and Caleb E. Finch, Aging: A Natural History (1995).
Meaning of AGING in English
Britannica English vocabulary. Английский словарь Британика. 2012