Timeline of senescence research

This page is a timeline of senescence research, including major theories, breakthroughs and organizations. "Senescence" here refers to "Ageing" rather than the phenomena of cellular senescence, which is a change in cell state associated with ageing, cancer prevention, wound healing, regeneration and embryonic/placenta development.

Full timeline
Year/periodType of EventEventLocation
c. 99 BC – c. 55 BCTheoryRoman poet and philosopher Lucretius argues that aging and death are beneficial because they make room for the next generation. This view will persist among biologists well into the 20th century.[1]
5th centuryTheoryEarly formulations, described by Hippocrates' system of four humours, theorize old age as a consequence of the gradual consumption of the innate heat with the inevitable loss of body moisture.[2]Greece
1825DevelopmentBenjamin Gompertz proposes an exponential increase in death rates with age, giving birth to what later will be called The Gompertz-Makeham law [3][4][5]
1891TheoryAugust Weismann proposes the first formal programmed aging theory as an evolutionary explanation of aging driven by group selection. His argument is that aging evolved to the advantage of the species (e.g., by replacing worn out individuals with younger ones), not the individual.[6][7]
1908TheoryMax Rubner describes his rate-of-living theory, which proposes that a slow metabolism increases an animal's longevity. It states that fast basal metabolic rate corresponds to short maximum life span.[8][9]
1913OrganizationThe Life Extension Institute is inaugurated as a longevity research center, with US president William Howard Taft as chairman.[10][11]U.S.A.
1928TheoryRaymond Pearl describes the Rate Of Living Hypothesis as an expansion of the earlier theory by Max Rubner. It states that organisms with a high metabolic rate have shorter lives.[12]
1934DiscoveryMary Crowell and Clive McCay of Cornell University discover that calorie restriction can extend lifespan twofold in rats.[13]
1945–1949DevelopmentThe advent of molecular biology changes the theoretical perception of aging dramatically, as the precise molecular structure of proteins and genetic material becomes known.[11]U.S.A.
1950sTheoryDenham Harman presents his free radical theory of aging, which states that organisms age over time due to the accumulation of damage from free radicals in the body.[12]
1952TheoryPeter Medawar formulates the first modern theory of mammal aging, known as mutation accumulation, whereby the mechanism of action involves random, detrimental germline mutations of a kind that happen to show their effect only late in life.[1]
1957TheoryGeorge C. Williams proposes the today called antagonistic pleiotropy hypothesis (AP) for the evolution of aging. It occurs when one gene controls for more than one phenotypic trait where at least one of these is beneficial to the organism's fitness and at least one is detrimental, thus accumulating damage.[1][14]
1958TheoryG. Failla and Leó Szilárd propose the somatic mutation theory, which suggests that aging is caused by random DNA damage in somatic cells and that the extent of damage is enhanced by radiation.[11]
1961TheoryAmerican anatomist Leonard Hayflick demonstrates that a population of normal human fetal cells in a cell culture will divide between 40 and 60 times before entering a senescence phase. This process will be known later as the Hayflick limit.[15][16][17]Philadelphia
1965–1969DiscoveryThe strong effect of age on DNA methylation levels is discovered,[18] thus rendering it an accurate biological clock in humans and chimpanzees.[19]
1967TheoryC. Alexander sets the grounds of the DNA damage theory of aging by suggesting that DNA damage, as distinct from mutation, is the primary cause of aging.[20] This theory becomes stronger through further experimental support during the following decades.[21][22]
1969BookAmerican physician Roy Walford publishes The Immunologic Theory of Aging, contributing to the basis for many current ideas about immunological aging.[23]
1974OrganizationThe National Institute on Aging (NIA) is formed as a division of the U.S. National Institutes of Health (NIH), with the purpose of conducting research on aging process and age-related diseases and disseminating information on health and research advances, among other aims.[24][25]Baltimore, U.S.A.
1975–1984DiscoveryElizabeth Blackburn discovers the unusual nature of telomeres, with their simple repeated DNA sequences composing chromosome ends.[26][27] Some years later Blackburn, Carol Greider and Jack Szostak discover how chromosomes are protected by telomeres and the enzyme telomerase, for which they receive the 2009 Nobel Prize in Physiology or Medicine.[28] Further experiments establish the role of telomere shortening in cellular aging and telomerase reactivation in cell immortalization.[29]
1977TheoryThomas Kirkwood proposes the third mainstream theory of ageing, the disposable soma, which states that organisms only have a limited amount of energy that has to be divided between reproductive activities and the maintenance of the non-reproductive aspects of the organism.[30]
1990OrganizationThe Gerontology Research Group (GRG) is founded as a global group of researchers in various fields that verifies and tracks supercentenarians. It also aims to further gerontology research with a goal of reversing or slowing aging.[31][32]Los Angeles, (UCLA)
1990-1995DevelopmentThe term negligible senescence is first used by professor Caleb Finch to describe organisms such as lobsters and hydras, which do not show symptoms of aging.[33]
1991TheoryLeonid A. Gavrilov and Natalia S. Gavrilova apply the principles of reliability theory to human biology, proposing a reliabity theory of aging which is based on the premise that humans are born in a highly defective state. According to the model, this is then made worse by environmental and mutational damage, and survival of the organism depends on redundancy.[34][35]
1993DiscoveryCynthia Kenyon discovers that a single-gene mutation (Daf-2) can double the lifespan of nematode Caenorhabditis elegans and that this can be reversed by a second mutation in daf-16m.[36][37]
1994BookLeonard Hayflick publishes How and Why we Age.[38]
1995DevelopmentDetection of senescent cells using a cytochemical assay is first described.[39]
2003OrganizationAubrey de Grey and David Gobel form the Methuselah Foundation, which gives financial grants to anti-aging research projects.[40]Springfield, Virginia, U.S.A.
2009OrganizationDe Grey and several others found the SENS Research Foundation with aims at conducting research into aging and funding other anti-aging research projects at various universities.[41][42][43]Mountain View, California, U.S.A
2010AchievementHarvard scientists reverse aging process in mice through reactivation of telomerase.[44]U.S.A.
2013OrganizationGoogle announces Calico, with the purpose of harnessing new technologies to increase scientific understanding of the biology of aging.[45]San Francisco, U.S.A
2017DiscoveryScientists knock out autophagy in the neurons of older worms resulting in a 50% boost to total longevity.[46]

See also

References
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  3. "Gompertz, Benjamin" . Dictionary of National Biography. London: Smith, Elder & Co. 1885–1900.
  4. Gompertz, B. (1825). "On the Nature of the Function Expressive of the Law of Human Mortality, and on a New Mode of Determining the Value of Life Contingencies". Philosophical Transactions of the Royal Society. 115: 513–585. doi:10.1098/rstl.1825.0026.
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  9. Rubner, M. (1908). Das Problem det Lebensdaur und seiner beziehunger zum Wachstum und Ernarnhung. Munich: Oldenberg.
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  14. Williams, G.C. (1957). "Pleiotropy, natural selection and the evolution of senescence" (PDF). Evolution. 11 (4): 398–411. doi:10.2307/2406060. JSTOR 2406060. Archived from the original (PDF) on 13 July 2006. Paper in which Williams describes his theory of antagonistic pleiotropy.
  15. "Will the Hayflick limit keep us from living forever?". 11 May 2009.
  16. Hayflick L, Moorhead PS (1961). "The serial cultivation of human diploid cell strains". Exp Cell Res. 25 (3): 585–621. doi:10.1016/0014-4827(61)90192-6. PMID 13905658.
  17. Hayflick L. (1965). "The limited in vitro lifetime of human diploid cell strains". Exp. Cell Res. 37 (3): 614–636. doi:10.1016/0014-4827(65)90211-9. PMID 14315085.
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  21. Bernstein C, Bernstein H (1991). Aging, Sex, and DNA Repair. San Diego CA: Academic Press. ISBN 978-0123960030.
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  23. Effros RB (2005). "Roy Walford and the immunologic theory of aging". Immun Ageing. 2 (1): 7. doi:10.1186/1742-4933-2-7. PMC 1131916. PMID 15850487.
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  26. "ELIZABETH BLACKBURN: TELOMERES AND TELOMERASE".
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  40. Methuselah Foundation - About
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