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The mutation accumulation theory of aging was first proposed by Peter Medawar in 1952 as an evolutionary explanation for biological aging and the associated decline in fitness that accompanies it. [1] Medawar used the term 'senescence' to refer to this process.
The somatic mutation theory of ageing states that accumulation of mutations in somatic cells is the primary cause of aging. A comparison of somatic mutation rate across several mammal species found that the total number of accumulated mutations at the end of lifespan was roughly equal across a broad range of lifespans. [16]
Biogerontology should not be confused with geriatrics, which is a field of medicine that studies the treatment of existing disease in aging people, rather than the treatment of aging itself. There are numerous theories of aging, and no one theory has been entirely accepted.
Senescence (/ s ɪ ˈ n ɛ s ə n s /) or biological aging is the gradual deterioration of functional characteristics in living organisms. Whole organism senescence involves an increase in death rates or a decrease in fecundity with increasing age, at least in the later part of an organism's life cycle.
Progeria is another example of a disease that may be related to cell senescence. The disease is thought to be caused by mutations in the DNA damage response, telomere shortening, or a combination of the two. [82] Progeroid syndromes are all examples of aging diseases where cell senescence appears to be implicated.
The DNA damage theory of aging proposes that aging is a consequence of unrepaired accumulation of naturally occurring DNA damage. Damage in this context is a DNA alteration that has an abnormal structure. Although both mitochondrial and nuclear DNA damage can contribute to aging, nuclear DNA is the main subject of this analysis.
Modern theories on the evolution of aging include the following: Mutation accumulation is a theory formulated by Peter Medawar in 1952 to explain how evolution would select for aging. Essentially, aging is never selected against, as organisms have offspring before the mortal mutations surface in an individual.
Genetics of aging is generally concerned with life extension associated with genetic alterations, rather than with accelerated aging diseases leading to reduction in lifespan. The first mutation found to increase longevity in an animal was the age-1 gene in Caenorhabditis elegans .