Senescence - Theories of Aging

Theories of Aging

The exact etiology of senescence is still largely unclear and yet to be discovered. The process of senescence is complex, and may derive from a variety of different mechanisms and exist for a variety of different reasons. However, senescence is not universal, and scientific evidence suggests that cellular senescence evolved in certain species because it prevents the onset of cancer. In a few simple species, such as Hydra, senescence is negligible and cannot be detected.

All such species have no "post-mitotic" cells; they reduce the effect of damaging free radicals by cell division and dilution. Another related mechanism is that of the biologically immortal planarian flatworms, which have “apparently limitless regenerative capacity fueled by a population of highly proliferative adult stem cells.” These organisms are biologically immortal but not immortal in the traditional sense as they are nonetheless susceptible to trauma and infectious and non-infectious disease. Moreover, average lifespans can vary greatly within and between species. This suggests that both genetic and environmental factors contribute to aging. It has been said, for example, that exposure to ultraviolet light elevates accumulation of free-radical damage.

In general, theories that explain senescence have been divided between the programmed and stochastic theories of aging. Programmed theories imply that aging is regulated by biological clocks operating throughout the lifespan. This regulation would depend on changes in gene expression that affect the systems responsible for maintenance, repair, and defense responses. The Reproductive-Cell Cycle Theory suggests that aging is caused by changes in hormonal signaling over the lifespan. Stochastic theories blame environmental impacts on living organisms that induce cumulative damage at various levels as the cause of aging, examples of which ranging from damage to DNA, damage to tissues and cells by oxygen radicals (widely known as free radicals countered by the even more well-known antioxidants), and cross-linking.

However, aging is seen as a progressive failure of homeodynamics (homeostasis) involving genes for the maintenance and repair, stochastic events leading to molecular damage and molecular heterogeneity, and chance events determining the probability of death. Since complex and interacting systems of maintenance and repair comprise the homeodynamic (old term: homeostasis) space of a biological system, aging is considered to be a progressive shrinkage of homeodynamic space mainly due to increased molecular heterogeneity.

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