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Senescence, or aging, is a biological term deriving from the Latin root word senex (“old man” or “old age”) and refers to the period following the development phase of a living organism, during which various processes cause it to age, deteriorate, and die. The period of senescence begins when an organism reaches sexual maturity and ends with the organism's death. For humans, senescence begins at about age 28 and ends at about age 85 under optimal living conditions.

The length of senescence is in large part genetically determined and is species-specific, correlating closely with the average life expectancy for any given species, with longer-lived species having a more prolonged period of senescence. One theory of aging states that this innate aging process is caused by the release of highly reactive molecules called “free radicals,” which arise from the processes of normal metabolism as well as from such external sources as chemical exposure, sunlight, smoking, or other environmental damage. Over time, these unstable compounds interact and bind with other molecules in the organism, gradually and cumulatively causing irreversible harm to cellular DNA, mitochondria, and cell membranes.

Senescence occurs at the cellular level when cells lose their ability to divide, or suffer “replicative senescence,” as the organism steadily loses the ability to respond to, or repair, damage caused by stress, injury, or disease. In humans this natural biological limit occurs after about 50 cell divisions, and is called the “Hayflick limit” in honor of the scientist who first observed this phenomenon in 1961. In contrast, for mice (a shorter-lived species than humans), cells typically divide only 10 times. In both plants and animals, each chromosome has at its end a specialized nucleoprotein complex (a “telomere”), which helps to protect, replicate, and stabilize the chromosome ends, allowing them to be repaired when damaged. Replicative senescence is thought to be caused in part because the telom-eres at the ends of cells become shorter each time the cell divides, until it can no longer divide and replicate itself. Senescence progresses as more and more cells across the organism reach their Hayflick limits and the body's cells are increasingly unable to reproduce or repair themselves. The remaining length of an organism's telomere sequences at any given point in time therefore serves as a natural “clock” or measure of how far senescence has progressed for that individual.

In addition to being affected by inherent aging processes, the length of senescence is also affected by the level of cell and tissue damage (and resulting DNA damage) that an individual organism experiences during its lifetime due to such environmental factors as food availability, temperature or light changes, disease or injury, or prédation. For all living organisms, then, better nutrition, shelter, treatment of diseases, and safety from physical injury will help to reduce cellular damage and to allow the upper natural limits of the senescence period for that species to be reached.

HelenSalmon
Crews, D. E. (2003). Human senescence: Evolutionary and biocultural perspectives. New York: Cambridge University Press. http://dx.doi.org/10.1017/CBO9780511542350
Harman,

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