In the past, there has been a tendency to confuse aging with diseases that are frequently associated with old age. It is, however, important to clearly distinguish the biochemical and physiological processes occurring with the onset of years from pathological conditions, for example cancer, arteriosclerosis (a generic term for several diseases in which the arterial wall becomes thickened and loses elasticity due to, for example, fatty deposits) and neurological disorders such as Alzheimer's disease. It was Fritz Verzar (1886-1979), Swiss gerontologist, who said that "Old age is not an illness; it is a continuation of life with decreasing capacities for adaptation." This view, that aging is a progressive failure of the body's homeostatic adaptive responses, gained wide acceptance only recently.
The obvious characteristics of old age are well known: greying and loss of hair, loss of teeth, wrinkling of the skin, decreased muscle mass and increased fat deposits. The physiological signs of aging are the gradual deterioration in function and capacity to respond to environmental stress. Thus basic kidney and digestive metabolic rates decrease, as does the ability to maintain a constant internal environment despite changes in temperature, diet and oxygen supply. These manifestations of aging are related to a decrease in the actual number of cells in the body (100,000 brain cells are lost each day) and to the disordered functioning of the cells that remain.
The extracellular components of tissues also change with age. Collagen fibres, responsible for the strength of tendons, increase in number and change in quality with aging. These changes within the fibres of arterial walls due to aging can be as much responsible for the loss of elasticity as those of the pathological condition culminating in arteroisclerosis. Elastin, another constituent of the intercellular matrix, is responsible for the elasticity of blood vessels and skin. In old age it thickens, fragments, and acquires a greater affinity for calcium. All these changes can also be associated with arteriosclerosis.
Most cells are not able to divide indefinitely. Several kinds of cells in the body, for example heart cells, skeletal muscle cells and neurons are incapable of replication. Experiments have also proved that many other cell types are limited in the number of cell divisions that they are able to perform. Embryonic fibroblast cells grown outside the body divide only about 50 times and then stop. Other experiments have shown that the number of cell divisions correlates with the age of the cell donor. The finite lifetime of cultured human cells has been observed in many normal cell types including skin, brain, liver and smooth muscle. No exception has been found to the general rule that normal cells possess a finite capacity to divide. The number of divisions also correlates with the normal lifespan of different species from which the cells are obtained-strong evidence that the cessation of mitosis is a normal, genetically programmed event.
Just as the factors that limit the life of an individual cell are unknown, so are those that restrict the growth or life of a tissue or organ. In women, at menopause the ovary ceases to function. Certain ovarian cells die long before the rest of the female body. One can speculate that similar mechanisms determine longevity. Some investigators have studied aging from the standpoint of immunology. The ability of a human being to develop antibodies is thought to diminish with age. Senescence, according to researchers, results in the older person's immunological system having a "shotgun" rather than a specific, response to a foreign protein. This shotgun response may include an autoimmune reaction that attacks and gradually destroys the individual's own normal tissue and organs.
Most gerontologists now believe that aging is a manifestation of the genetic coding within the cells of an organism. As a logical extension of the concept of development that begins from the moment of conception, aging must be part of the ongoing genetic expression of events that guide human organisms through embryological and fetal development, through childhood changes, adolescence and maturity. There are three general hypotheses that have been used as a basis for additional research. The first hypothesis proposes that, as time passes, the information-processing apparatus of cells begins to make more and more errors. As a result, faulty enzymes lead to a decline in the functional capability of the cells. Experiments designed to study protein synthesis in aging cells have not produced evidence that supports this hypothesis. The second hypothesis argues that many of the genes along the DNA molecule are repeated in identical sequences, making the genetic message very redundant. When an active gene is damaged, it may be replaced by one of the copies. Thus, as a person lives, the copies are gradually used up, errors accumulate, and functional losses result. According to this hypothesis, the greater the redundancy, the longer the lifespan. This hypothesis is also not substantiated by much evidence, although recent advances in the human genome analysis may provide more information.
The third hypothesis proposes that aging is a continuation of a normal sequence of genetic signals that regulate development. This idea suggests that aging genes are activated in the proper sequence, which causes a slowing down of biochemical pathways that are expressed in the recognizable changes of aging. There are two cell lines that are known to escape the inevitability of aging and death. These are germ cells and cancer cells. Perhaps these cell lines share a common genetic mechanism that makes them immortal. Fertilization may be a process that resets or reprograms a cell's clock by reshuffling the genetic information. These mechanisms make certain that each member of the species is programmed to die but ensure that the species will survive. Taking this view, one can look at an organism as a carrier of immortal germ cells and death as an effective survival strategy for the species. Since viruses can also reshuffle the genetic information of cells by integrating into the DNA, it is possible that viruses can cause cells to become "immortal" and cancerous.
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