This theory, which was first introduced by Dr. Recent studies show that cross-linking reactions are involved in the age related changes in the studied proteins ( 9). According to this theory, an accumulation of cross-linked proteins damages cells and tissues, slowing down bodily processes resulting in aging. The cross-linking theory of aging was proposed by Johan Bjorksten in 1942 ( 8). Rollo proposes a modified version of Pearl’s rate of living theory emphasizing the hard-wired antagonism of growth (TOR) and stress resistance (FOXO) ( 7). The rate-of-living theory of aging while helpful is not completely adequate in explaining the maximum life span ( 6).Dr. The greater an organism’s rate of oxygen basal metabolism, the shorter its life span ( 5). August Weismann, a German biologist, in 1882, it sounds perfectly reasonable to many people even today, because this is what happens to most familiar things around them. So the wear and tear theory of aging was first introduced by Dr. Like components of an aging car, parts of the body eventually wear out from repeated use, killing them and then the body. Cells and tissues have vital parts that wear out resulting in aging. The damage or error theory include 1) Wear and tear theory. Although direct causal relationships have not been established for all these detrimental outcomes, the immune system has been at least indirectly implicated ( 4). Indeed, dysregulated immune response has been linked to cardiovascular disease, inflammation, Alzheimer’s disease (AD), and cancer. For example, as one grows older, antibodies lose their effectiveness, and fewer new diseases can be combated effectively by the body, which causes cellular stress and eventual death ( 3). It is well documented that the effectiveness of the immune system peaks at puberty and gradually declines thereafter with advance in age. The immune system is programmed to decline over time, which leads to an increased vulnerability to infectious disease and thus aging and death. van Heemst discusses the potential mechanism underlying IIS and aging process( 2). Recent studies confirm that aging is hormonally regulated and that the evolutionarily conserved insulin/IGF-1 signaling (IIS) pathway plays a key role in the hormonal regulation of aging. Biological clocks act through hormones to control the pace of aging. Davidovic et al discuss the role of genetic instability in aging and dynamics of the aging process ( 1). Aging is the result of a sequential switching on and off of certain genes, with senescence being defined as the time when age-associated deficits are manifested. The programmed theory has three sub-categories: 1) Programmed Longevity. The damage or error theories emphasize environmental assaults to living organisms that induce cumulative damage at various levels as the cause of aging. This regulation would depend on changes in gene expression that affect the systems responsible for maintenance, repair and defense responses. The programmed theories imply that aging follows a biological timetable, perhaps a continuation of the one that regulates childhood growth and development. Modern biological theories of aging in humans fall into two main categories: programmed and damage or error theories. The traditional aging theories hold that aging is not an adaptation or genetically programmed. Many theories have been proposed to explain the process of aging, but neither of them appears to be fully satisfactory ( 1). However, in spite of recent advances in molecular biology and genetics, the mysteries that control human lifespan are yet to be unraveled. Why do we age? When do we start aging? What is the aging marker? Is there a limit to how old we can grow? These questions are often pondered by the mankind in the past couple of hundred years.
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