Difference between revisions of "Timeline of senescence research"

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! Year/period !! Type of Event !! Event !! Location  
 
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| c. 99 BC – c. 55 BC|| Theory || Roman poet and philosopher [[wikipedia:Lucretius|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.<ref name=the-evolution-of-aging>{{cite magazine |author1=Daniel Fabian |author2=Thomas Flatt |title=The Evolution of Aging |url=http://www.nature.com/scitable/knowledge/library/the-evolution-of-aging-23651151 |magazine=Nature |location= |publisher= |date= |access-date= }}</ref> ||
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| c. 99 BC – c. 55 BC|| Scientific development (theory) || Roman poet and philosopher [[wikipedia:Lucretius|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.<ref name=the-evolution-of-aging>{{cite magazine |author1=Daniel Fabian |author2=Thomas Flatt |title=The Evolution of Aging |url=http://www.nature.com/scitable/knowledge/library/the-evolution-of-aging-23651151 |magazine=Nature |location= |publisher= |date= |access-date= }}</ref> ||
 
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|5th century || Theory ||Early formulations, described by  [[wikipedia:Hippocrates|Hippocrates]]' system of four [[wikipedia:Humorism|humours]], theorize old age as a consequence of the gradual consumption of the innate heat with the inevitable loss of body moisture.<ref name=history-of-research/>  || Greece
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|5th century || Scientific development (theory) ||Early formulations, described by  [[wikipedia:Hippocrates|Hippocrates]]' system of four [[wikipedia:Humorism|humours]], theorize old age as a consequence of the gradual consumption of the innate heat with the inevitable loss of body moisture.<ref name=history-of-research/>  || Greece
 
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|1825 || Development || [[wikipedia:Benjamin Gompertz|Benjamin Gompertz]] proposes an exponential increase in death rates with age, giving birth to what later will be called The [[wikipedia:Gompertz-Makeham law of mortality|Gompertz-Makeham law]] <ref>{{cite DNB|wstitle=Gompertz, Benjamin}}</ref><ref>{{cite journal |last=Gompertz |first=B. |year=1825 |title=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 |journal=Philosophical Transactions of the Royal Society |volume=115 |issue= |pages=513–585 |id= |url=http://visualiseur.bnf.fr/Visualiseur?Destination=Gallica&O=NUMM-55920 |doi=10.1098/rstl.1825.0026}}
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|1825 || Scientific development || [[wikipedia:Benjamin Gompertz|Benjamin Gompertz]] proposes an exponential increase in death rates with age, giving birth to what later will be called The [[wikipedia:Gompertz-Makeham law of mortality|Gompertz-Makeham law]] <ref>{{cite DNB|wstitle=Gompertz, Benjamin}}</ref><ref>{{cite journal |last=Gompertz |first=B. |year=1825 |title=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 |journal=Philosophical Transactions of the Royal Society |volume=115 |issue= |pages=513–585 |id= |url=http://visualiseur.bnf.fr/Visualiseur?Destination=Gallica&O=NUMM-55920 |doi=10.1098/rstl.1825.0026}}
 
</ref><ref name="Leonid">Leonid A. Gavrilov & Natalia S. Gavrilova (1991) The Biology of Life Span: A Quantitative Approach. New York: Harwood Academic Publisher, ISBN 3-7186-4983-7</ref>||
 
</ref><ref name="Leonid">Leonid A. Gavrilov & Natalia S. Gavrilova (1991) The Biology of Life Span: A Quantitative Approach. New York: Harwood Academic Publisher, ISBN 3-7186-4983-7</ref>||
 
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| 1891 || Theory || [[wikipedia:August Weismann|August 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.<ref>{{cite web|url=http://www.programmed-aging.org/programmed_aging_theory_FAQ.html|title=Biological Aging Theory - Frequently asked Questions and Answers}}</ref><ref>{{cite web |title=A Weismann| URL=http://www.senescence.info/evolution_of_aging.html}}</ref> ||
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| 1891 || Scientific development (theory) || [[wikipedia:August Weismann|August 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.<ref>{{cite web|url=http://www.programmed-aging.org/programmed_aging_theory_FAQ.html|title=Biological Aging Theory - Frequently asked Questions and Answers}}</ref><ref>{{cite web |title=A Weismann| URL=http://www.senescence.info/evolution_of_aging.html}}</ref> ||
 
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|1908|| Theory || [[wikipedia:Max Rubner|Max Rubner]] describes his ''[[wikipedia:rate-of-living theory|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.<ref>{{cite journal |author1=Michael Ristow |author2=Kathrin Schmeisser |date= |title=Mitohormesis: Promoting Health and Lifespan by Increased Levels of Reactive Oxygen Species (ROS) |journal= Dose Response|publisher= |volume= 12|issue= |pages= 288–341|doi= 10.2203/dose-response.13-035.Ristow|pmc=4036400 |pmid= 24910588 |year=2014}}</ref><ref>Rubner, M. (1908). Das Problem det Lebensdaur und seiner beziehunger zum Wachstum und Ernarnhung. Munich: Oldenberg.</ref> ||  
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| 1908 || Scientific development (theory) || [[wikipedia:Max Rubner|Max Rubner]] describes his ''[[wikipedia:rate-of-living theory|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.<ref>{{cite journal |author1=Michael Ristow |author2=Kathrin Schmeisser |date= |title=Mitohormesis: Promoting Health and Lifespan by Increased Levels of Reactive Oxygen Species (ROS) |journal= Dose Response|publisher= |volume= 12|issue= |pages= 288–341|doi= 10.2203/dose-response.13-035.Ristow|pmc=4036400 |pmid= 24910588 |year=2014}}</ref><ref>Rubner, M. (1908). Das Problem det Lebensdaur und seiner beziehunger zum Wachstum und Ernarnhung. Munich: Oldenberg.</ref> ||  
 
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|1913 ||Organization|| The [[wikipedia:Life Extension Institute|Life Extension Institute]] is inaugurated as a longevity research center, with US president [[wikipedia:William Howard Taft|William Howard Taft]] as chairman.<ref>{{cite book|last1=Hamowy|first1=Ronald|title=Government and Public Health in America|url=https://books.google.com.ar/books?id=TSn0SVM3GRcC&pg=PA430&lpg=PA430&dq=%221913%22+%22+Life+Extension+Institute+%22&source=bl&ots=OQ1ROt5qc8&sig=q-RR0XyiQ2phecDuQWf581q6RxY&hl=es&sa=X&ved=0ahUKEwikvIOn9oXRAhWPPpAKHURcBUQQ6AEIPjAD#v=onepage&q=%221913%22%20%22%20Life%20Extension%20Institute%20%22&f=false|accessdate=21 December 2016}}</ref><ref name=ilia-stambler/>||U.S.A.
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| 1913 || Organization || The [[wikipedia:Life Extension Institute|Life Extension Institute]] is inaugurated as a longevity research center, with US president [[wikipedia:William Howard Taft|William Howard Taft]] as chairman.<ref>{{cite book|last1=Hamowy|first1=Ronald|title=Government and Public Health in America|url=https://books.google.com.ar/books?id=TSn0SVM3GRcC&pg=PA430&lpg=PA430&dq=%221913%22+%22+Life+Extension+Institute+%22&source=bl&ots=OQ1ROt5qc8&sig=q-RR0XyiQ2phecDuQWf581q6RxY&hl=es&sa=X&ved=0ahUKEwikvIOn9oXRAhWPPpAKHURcBUQQ6AEIPjAD#v=onepage&q=%221913%22%20%22%20Life%20Extension%20Institute%20%22&f=false|accessdate=21 December 2016}}</ref><ref name=ilia-stambler/>|| {{w|United States}}
 
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| 1928 || Theory || [[wikipedia:Raymond Pearl|Raymond Pearl]] describes the ''Rate Of Living Hypothesis'' as an expansion of the earlier theory by [[wikipedia:Max Rubner|Max Rubner]]. It states that organisms with a high metabolic rate have shorter lives.<ref name=oxidative-stress>{{cite book |author= David Costantini |title=Oxidative Stress and Hormesis in Evolutionary Ecology and Physiology |url=https://books.google.com.ar/books?id=rTe8BAAAQBAJ&pg=PA306&dq=Rate+Of+Living+Hypothesis&hl=es&sa=X&ved=0ahUKEwjui-iU5tDMAhXJIJAKHe4lBSMQ6AEILDAC#v=onepage&q=Pearl&f=false |location= |publisher= |page=306 |date= |isbn=}}</ref>||
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| 1928 || Scientific development (theory) || [[wikipedia:Raymond Pearl|Raymond Pearl]] describes the ''Rate Of Living Hypothesis'' as an expansion of the earlier theory by [[wikipedia:Max Rubner|Max Rubner]]. It states that organisms with a high metabolic rate have shorter lives.<ref name=oxidative-stress>{{cite book |author= David Costantini |title=Oxidative Stress and Hormesis in Evolutionary Ecology and Physiology |url=https://books.google.com.ar/books?id=rTe8BAAAQBAJ&pg=PA306&dq=Rate+Of+Living+Hypothesis&hl=es&sa=X&ved=0ahUKEwjui-iU5tDMAhXJIJAKHe4lBSMQ6AEILDAC#v=onepage&q=Pearl&f=false |location= |publisher= |page=306 |date= |isbn=}}</ref>||
 
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| 1934 || Discovery || Mary Crowell and Clive McCay of Cornell University discover that [[wikipedia:calorie restriction|calorie restriction]] can extend lifespan twofold in rats.<ref>{{cite book |last= Fossel |first=Michael |date= |title=The Telomerase Revolution: The Enzyme That Holds the Key to Human Aging |url= |location= |publisher= |page= |isbn=}}</ref>||
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| 1934 || Scientific development (theory) || Mary Crowell and Clive McCay of Cornell University discover that [[wikipedia:calorie restriction|calorie restriction]] can extend lifespan twofold in rats.<ref>{{cite book |last= Fossel |first=Michael |date= |title=The Telomerase Revolution: The Enzyme That Holds the Key to Human Aging |url= |location= |publisher= |page= |isbn=}}</ref>||
 
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|1945–1949|| Development || The advent of [[wikipedia:molecular biology|molecular biology]] changes the theoretical perception of aging dramatically, as the precise molecular structure of [[wikipedia:proteins|proteins]] and genetic material becomes known.<ref name=ilia-stambler/> || U.S.A.
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|1945–1949|| Scientific development || The advent of [[wikipedia:molecular biology|molecular biology]] changes the theoretical perception of aging dramatically, as the precise molecular structure of [[wikipedia:proteins|proteins]] and genetic material becomes known.<ref name=ilia-stambler/> || {{w|United States}}
 
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|1950s || Theory ||  [[wikipedia:Denham Harman|Denham Harman]] presents his ''[[wikipedia:free radical theory of aging|free radical theory of aging]]'', which states that organisms age over time due to the accumulation of damage from free radicals in the body.<ref name=oxidative-stress/>||
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|1950s || Scientific development (theory) ||  [[wikipedia:Denham Harman|Denham Harman]] presents his ''[[wikipedia:free radical theory of aging|free radical theory of aging]]'', which states that organisms age over time due to the accumulation of damage from free radicals in the body.<ref name=oxidative-stress/>||
 
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| 1952 || Theory || [[wikipedia:Peter Medawar|Peter Medawar]] formulates the first modern theory of mammal aging, known as ''[[wikipedia:mutation accumulation|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.<ref name=the-evolution-of-aging/> ||
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| 1952 || Scientific development (theory) || [[wikipedia:Peter Medawar|Peter Medawar]] formulates the first modern theory of mammal aging, known as ''[[wikipedia:mutation accumulation|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.<ref name=the-evolution-of-aging/> ||
 
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| 1957 || Theory|| [[wikipedia:George C. Williams (biologist)|George C. Williams]] proposes the today called ''[[wikipedia:antagonistic pleiotropy hypothesis|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.<ref name=the-evolution-of-aging/><ref name="williams">{{cite journal|doi=10.2307/2406060 |author=Williams, G.C.|title=Pleiotropy, natural selection and the evolution of senescence|journal=Evolution|volume=11|issue=4|pages=398–411 |year=1957|format=PDF|url=http://www.telomere.org/Downloads/Williams_searchable.pdf|jstor=2406060}} Paper in which Williams describes his theory of antagonistic pleiotropy.</ref> ||
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| 1957 || Scientific development (theory) || [[wikipedia:George C. Williams (biologist)|George C. Williams]] proposes the today called ''[[wikipedia:antagonistic pleiotropy hypothesis|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.<ref name=the-evolution-of-aging/><ref name="williams">{{cite journal|doi=10.2307/2406060 |author=Williams, G.C.|title=Pleiotropy, natural selection and the evolution of senescence|journal=Evolution|volume=11|issue=4|pages=398–411 |year=1957|format=PDF|url=http://www.telomere.org/Downloads/Williams_searchable.pdf|jstor=2406060}} Paper in which Williams describes his theory of antagonistic pleiotropy.</ref> ||
 
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|1958 || Theory || [[wikipedia:Gioacchino Failla|G. Failla]] and [[wikipedia:Leó Szilárd|Leó Szilárd]] propose the ''[[wikipedia:somatic mutation theory|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.<ref name=ilia-stambler/> ||
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|1958 || Scientific development (theory) || [[wikipedia:Gioacchino Failla|G. Failla]] and [[wikipedia:Leó Szilárd|Leó Szilárd]] propose the ''[[wikipedia:somatic mutation theory|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.<ref name=ilia-stambler/> ||
 
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|1961 || Theory || American anatomist [[wikipedia:Leonard Hayflick|Leonard Hayflick]] demonstrates that a population of normal [[wikipedia:human fetal|human fetal]] cells in a [[wikipedia:cell culture|cell culture]] will divide between 40 and 60 times before entering a [[wikipedia:senescence|senescence]] phase. This process will be known later as the [[wikipedia:Hayflick limit|Hayflick limit]].<ref>{{cite web|url=http://science.howstuffworks.com/life/genetic/hayflick-limit.htm|title=Will the Hayflick limit keep us from living forever?}}</ref><ref name="pmid13905659">{{cite journal |vauthors=Hayflick L, Moorhead PS |title=The serial cultivation of human diploid cell strains |journal=Exp Cell Res |volume=25 |pages=585–621 |year=1961 |pmid=13905658 |doi=10.1016/0014-4827(61)90192-6 |issue=3}}</ref><ref>{{cite journal |author=Hayflick L. |title= The limited in vitro lifetime of human diploid cell strains |journal=Exp. Cell Res. |year=1965 |volume=37 |issue=3 |pages=614–636 |pmid= 14315085 |doi=10.1016/0014-4827(65)90211-9}}</ref>||[[wikipedia:Wistar Institute|Philadelphia]]  
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|1961 || Scientific development (theory) || American anatomist [[wikipedia:Leonard Hayflick|Leonard Hayflick]] demonstrates that a population of normal [[wikipedia:human fetal|human fetal]] cells in a [[wikipedia:cell culture|cell culture]] will divide between 40 and 60 times before entering a [[wikipedia:senescence|senescence]] phase. This process will be known later as the [[wikipedia:Hayflick limit|Hayflick limit]].<ref>{{cite web|url=http://science.howstuffworks.com/life/genetic/hayflick-limit.htm|title=Will the Hayflick limit keep us from living forever?}}</ref><ref name="pmid13905659">{{cite journal |vauthors=Hayflick L, Moorhead PS |title=The serial cultivation of human diploid cell strains |journal=Exp Cell Res |volume=25 |pages=585–621 |year=1961 |pmid=13905658 |doi=10.1016/0014-4827(61)90192-6 |issue=3}}</ref><ref>{{cite journal |author=Hayflick L. |title= The limited in vitro lifetime of human diploid cell strains |journal=Exp. Cell Res. |year=1965 |volume=37 |issue=3 |pages=614–636 |pmid= 14315085 |doi=10.1016/0014-4827(65)90211-9}}</ref>||[[wikipedia:Wistar Institute|Philadelphia]]  
 
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|1965–1969|| Discovery || The strong effect of age on [[wikipedia:DNA methylation|DNA methylation]] levels is discovered,<ref>{{cite journal | last1 = Berdyshev | first1 = G | last2 = Korotaev | first2 = G | last3 = Boiarskikh | first3 = G | last4 = Vaniushin | first4 = B | year = 1967 | title = Nucleotide composition of DNA and RNA from somatic tissues of humpback and its changes during spawning | url = | journal = Biokhimiia | volume = 31 | issue = | pages = 88–993 }}</ref> thus rendering it an accurate biological clock in humans and chimpanzees.<ref>{{Cite journal |author=Horvath S |title=DNA methylation age of human tissues and cell types |journal=Genome Biology |volume=14 |number=R115 |pages= R115|year=2013 |url=http://genomebiology.com/2013/14/10/r115|doi=10.1186/gb-2013-14-10-r115|pmid=24138928 |pmc=4015143}}</ref> ||
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|1965–1969|| Scientific development || The strong effect of age on [[wikipedia:DNA methylation|DNA methylation]] levels is discovered,<ref>{{cite journal | last1 = Berdyshev | first1 = G | last2 = Korotaev | first2 = G | last3 = Boiarskikh | first3 = G | last4 = Vaniushin | first4 = B | year = 1967 | title = Nucleotide composition of DNA and RNA from somatic tissues of humpback and its changes during spawning | url = | journal = Biokhimiia | volume = 31 | issue = | pages = 88–993 }}</ref> thus rendering it an accurate biological clock in humans and chimpanzees.<ref>{{Cite journal |author=Horvath S |title=DNA methylation age of human tissues and cell types |journal=Genome Biology |volume=14 |number=R115 |pages= R115|year=2013 |url=http://genomebiology.com/2013/14/10/r115|doi=10.1186/gb-2013-14-10-r115|pmid=24138928 |pmc=4015143}}</ref> ||
 
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|1967 || Theory || C. Alexander sets the grounds of the ''[[wikipedia:DNA damage theory of aging|DNA damage theory of aging]]'' by suggesting that DNA damage, as distinct from mutation, is the primary cause of aging.<ref>{{cite journal |author=Alexander P |title=The role of DNA lesions in the processes leading to aging in mice |journal=Symp. Soc. Exp. Biol. |volume=21 |pages=29–50 |year=1967 |pmid=4860956 }}</ref> This theory becomes stronger through further experimental support during the following decades.<ref>{{cite book |vauthors=Bernstein C, Bernstein H |title=Aging, Sex, and DNA Repair |publisher=Academic Press |location=San Diego CA |year=1991 |isbn=0123960037 }}</ref><ref>{{cite journal |vauthors=Ames BN, Gold LS |title=Endogenous mutagens and the causes of aging and cancer |journal=Mutat. Res. |volume=250 |issue=1-2 |pages=3–16 |year=1991 |pmid=1944345 |doi=10.1016/0027-5107(91)90157-j}}</ref> ||
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|1967 || Scientific development (theory) || C. Alexander sets the grounds of the ''[[wikipedia:DNA damage theory of aging|DNA damage theory of aging]]'' by suggesting that DNA damage, as distinct from mutation, is the primary cause of aging.<ref>{{cite journal |author=Alexander P |title=The role of DNA lesions in the processes leading to aging in mice |journal=Symp. Soc. Exp. Biol. |volume=21 |pages=29–50 |year=1967 |pmid=4860956 }}</ref> This theory becomes stronger through further experimental support during the following decades.<ref>{{cite book |vauthors=Bernstein C, Bernstein H |title=Aging, Sex, and DNA Repair |publisher=Academic Press |location=San Diego CA |year=1991 |isbn=0123960037 }}</ref><ref>{{cite journal |vauthors=Ames BN, Gold LS |title=Endogenous mutagens and the causes of aging and cancer |journal=Mutat. Res. |volume=250 |issue=1-2 |pages=3–16 |year=1991 |pmid=1944345 |doi=10.1016/0027-5107(91)90157-j}}</ref> ||
 
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|1969||Book||American physician [[wikipedia:Roy Walford|Roy Walford]] publishes ''The Immunologic Theory of Aging'', contributing to the basis for many current ideas about immunological aging.<ref>{{cite journal|title=Roy Walford and the immunologic theory of aging|doi=10.1186/1742-4933-2-7| pmc=1131916 | pmid=15850487|volume=2|year=2005|journal=Immun Ageing|pages=7|author=Effros RB}}</ref>||
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|1969|| Publication ||American physician [[wikipedia:Roy Walford|Roy Walford]] publishes ''The Immunologic Theory of Aging'', contributing to the basis for many current ideas about immunological aging.<ref>{{cite journal|title=Roy Walford and the immunologic theory of aging|doi=10.1186/1742-4933-2-7| pmc=1131916 | pmid=15850487|volume=2|year=2005|journal=Immun Ageing|pages=7|author=Effros RB}}</ref>||
 
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|  1974 || Organization || The [[wikipedia:National Institute on Aging|National Institute on Aging]] (NIA) is formed as a division of the U.S. [[wikipedia:National Institutes of Health|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.<ref>{{cite book|last1=Ofahengaue Vakalahi|first1=Halaevalu F.|last2=Simpson|first2=Gaynell M.|last3=Giunta|first3=Nancy|title=The Collective Spirit of Aging Across Cultures|page=20|url=https://books.google.com.ar/books?id=58XEBAAAQBAJ&pg=PA20&lpg=PA20&dq=%221974%22+%22National+Institute+on+Aging+%22&source=bl&ots=h5rgitHiKf&sig=W29lqL0xqia6j_EdPOGrioIvd58&hl=en&sa=X&ved=0ahUKEwi6kuXq9oXRAhXLDJAKHYgwA-oQ6AEINzAF#v=onepage&q=%221974%22%20%22National%20Institute%20on%20Aging%20%22&f=false|accessdate=21 December 2016}}</ref><ref>{{cite web |url=https://www.nia.nih.gov/ |title=National Institute of Aging}}</ref> || [[wikipedia:Baltimore|Baltimore]], U.S.A.
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|  1974 || Organization || The [[wikipedia:National Institute on Aging|National Institute on Aging]] (NIA) is formed as a division of the United States [[wikipedia:National Institutes of Health|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.<ref>{{cite book|last1=Ofahengaue Vakalahi|first1=Halaevalu F.|last2=Simpson|first2=Gaynell M.|last3=Giunta|first3=Nancy|title=The Collective Spirit of Aging Across Cultures|page=20|url=https://books.google.com.ar/books?id=58XEBAAAQBAJ&pg=PA20&lpg=PA20&dq=%221974%22+%22National+Institute+on+Aging+%22&source=bl&ots=h5rgitHiKf&sig=W29lqL0xqia6j_EdPOGrioIvd58&hl=en&sa=X&ved=0ahUKEwi6kuXq9oXRAhXLDJAKHYgwA-oQ6AEINzAF#v=onepage&q=%221974%22%20%22National%20Institute%20on%20Aging%20%22&f=false|accessdate=21 December 2016}}</ref><ref>{{cite web |url=https://www.nia.nih.gov/ |title=National Institute of Aging}}</ref> || {{w|United States}} ([[wikipedia:Baltimore|Baltimore]])
 
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| 1975–1984 ||Discovery || [[wikipedia:Elizabeth Blackburn|Elizabeth Blackburn]] discovers the unusual nature of telomeres, with their simple repeated DNA sequences composing chromosome ends.<ref>{{cite web|url=http://www.ibiology.org/ibioseminars/genetics-gene-regulation/elizabeth-blackburn-part-1.html|title=ELIZABETH BLACKBURN: TELOMERES AND TELOMERASE}}</ref><ref>{{cite journal |author=Blackburn AM |title=A tandemly repeated sequence at the termini of the extrachromosomal ribosomal RNA genes in Tetrahymena |journal=J. Mol. Biol. |volume=120 |issue=1 |pages=33–53 | date=March 1978 |doi=10.1016/0022-2836(78)90294-2 |pmid=642006 |first2=Joseph G.|last2=Gall }}</ref> Some years later Blackburn, [[wikipedia:Carol Greider|Carol Greider]] and [[wikipedia:Jack Szostak|Jack Szostak]] discover  how chromosomes are protected by telomeres and the enzyme [[wikipedia:telomerase|telomerase]], for which they receive the 2009 Nobel Prize in Physiology or Medicine.<ref>{{cite web|url=http://nobelprize.org/nobel_prizes/medicine/laureates/2009/press.html |title=The 2009 Nobel Prize in Physiology or Medicine - Press Release |publisher=Nobelprize.org |date=2009-10-05 |accessdate=2012-06-12}}</ref>  Further experiments establish the role of telomere shortening in [[wikipedia:cellular aging|cellular aging]] and telomerase reactivation in cell immortalization.<ref>{{cite news|title=Unravelling the secret of ageing |url=http://www.cosmosmagazine.com/features/unraveling-secret-ageing/ |work=COSMOS: The Science of Everything |date=October 5, 2009 |deadurl=yes |archiveurl=https://web.archive.org/web/20150114212810/http://cosmosmagazine.com/features/unraveling-secret-ageing/ |archivedate=January 14, 2015 }}</ref> ||
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| 1975–1984 || Scientific development || [[wikipedia:Elizabeth Blackburn|Elizabeth Blackburn]] discovers the unusual nature of telomeres, with their simple repeated DNA sequences composing chromosome ends.<ref>{{cite web|url=http://www.ibiology.org/ibioseminars/genetics-gene-regulation/elizabeth-blackburn-part-1.html|title=ELIZABETH BLACKBURN: TELOMERES AND TELOMERASE}}</ref><ref>{{cite journal |author=Blackburn AM |title=A tandemly repeated sequence at the termini of the extrachromosomal ribosomal RNA genes in Tetrahymena |journal=J. Mol. Biol. |volume=120 |issue=1 |pages=33–53 | date=March 1978 |doi=10.1016/0022-2836(78)90294-2 |pmid=642006 |first2=Joseph G.|last2=Gall }}</ref> Some years later Blackburn, [[wikipedia:Carol Greider|Carol Greider]] and [[wikipedia:Jack Szostak|Jack Szostak]] discover  how chromosomes are protected by telomeres and the enzyme [[wikipedia:telomerase|telomerase]], for which they receive the 2009 Nobel Prize in Physiology or Medicine.<ref>{{cite web|url=http://nobelprize.org/nobel_prizes/medicine/laureates/2009/press.html |title=The 2009 Nobel Prize in Physiology or Medicine - Press Release |publisher=Nobelprize.org |date=2009-10-05 |accessdate=2012-06-12}}</ref>  Further experiments establish the role of telomere shortening in [[wikipedia:cellular aging|cellular aging]] and telomerase reactivation in cell immortalization.<ref>{{cite news|title=Unravelling the secret of ageing |url=http://www.cosmosmagazine.com/features/unraveling-secret-ageing/ |work=COSMOS: The Science of Everything |date=October 5, 2009 |deadurl=yes |archiveurl=https://web.archive.org/web/20150114212810/http://cosmosmagazine.com/features/unraveling-secret-ageing/ |archivedate=January 14, 2015 }}</ref> ||
 
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|1977 || Theory|| [[wikipedia:Thomas Kirkwood|Thomas Kirkwood]] proposes the third mainstream theory of ageing, the ''[[wikipedia:disposable soma|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.<ref>{{cite book |last=Goldsmith  |first=Theodore |date= |title=The Evolution of Aging: How New Theories Will Change the Future of Medicine |url=https://books.google.com.ar/books?id=bCwC22mim4gC&pg=PA48&lpg=PA48&dq=%22Thomas+Kirkwood%22+%22Disposable+soma%22+%221977%22&source=bl&ots=JCdSwbtSVo&sig=Ht8Ttjq7KF_zPMvlhtxPbY_ZxHc&hl=en&sa=X&ved=0ahUKEwi5uqfCmqjOAhXHvJAKHWIlBrwQ6AEIPTAG#v=onepage&q=%22Thomas%20Kirkwood%22%20%22Disposable%20soma%22%20%221977%22&f=false |location= |publisher= |page=48 |isbn=}}</ref>||
+
|1977 || Scientific development (theory) || [[wikipedia:Thomas Kirkwood|Thomas Kirkwood]] proposes the third mainstream theory of ageing, the ''[[wikipedia:disposable soma|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.<ref>{{cite book |last=Goldsmith  |first=Theodore |date= |title=The Evolution of Aging: How New Theories Will Change the Future of Medicine |url=https://books.google.com.ar/books?id=bCwC22mim4gC&pg=PA48&lpg=PA48&dq=%22Thomas+Kirkwood%22+%22Disposable+soma%22+%221977%22&source=bl&ots=JCdSwbtSVo&sig=Ht8Ttjq7KF_zPMvlhtxPbY_ZxHc&hl=en&sa=X&ved=0ahUKEwi5uqfCmqjOAhXHvJAKHWIlBrwQ6AEIPTAG#v=onepage&q=%22Thomas%20Kirkwood%22%20%22Disposable%20soma%22%20%221977%22&f=false |location= |publisher= |page=48 |isbn=}}</ref>||
 
|-
 
|-
|1990 || Organization || The [[wikipedia:Gerontology Research Group |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.<ref>{{cite web |title=Keeping Track of the Oldest People in the World |url=http://www.smithsonianmag.com/science-nature/keeping-track-oldest-people-world-180951976/?no-ist |last=Nuwer |first=Rachel |publisher=Smithsonion.com |date=4 July 2014 |accessdate=3 January 2015}}</ref><ref>{{cite news |title=Supercentenarians giving researchers clues on longevity |url=http://articles.chicagotribune.com/2006-02-08/features/0602080100_1_guinness-world-records-oldest-people-supercentenarians |newspaper=Chicago Tribune |last=White |first=Gayle |agency=Cox News Service |date=8 February 2006 |accessdate=3 January 2015}}</ref> || [[wikipedia:Los Angeles|Los Angeles]], ([[wikipedia:UCLA|UCLA]])
+
|1990 || Organization || The [[wikipedia:Gerontology Research Group |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.<ref>{{cite web |title=Keeping Track of the Oldest People in the World |url=http://www.smithsonianmag.com/science-nature/keeping-track-oldest-people-world-180951976/?no-ist |last=Nuwer |first=Rachel |publisher=Smithsonion.com |date=4 July 2014 |accessdate=3 January 2015}}</ref><ref>{{cite news |title=Supercentenarians giving researchers clues on longevity |url=http://articles.chicagotribune.com/2006-02-08/features/0602080100_1_guinness-world-records-oldest-people-supercentenarians |newspaper=Chicago Tribune |last=White |first=Gayle |agency=Cox News Service |date=8 February 2006 |accessdate=3 January 2015}}</ref> || {{w|United States}} ([[wikipedia:UCLA|UCLA]])
 
|-
 
|-
|1990-1995 || Development || The term ''[[wikipedia:negligible senescence|negligible senescence]]'' is first used by professor [[wikipedia:Caleb Finch|Caleb Finch]] to describe organisms such as [[wikipedia:lobsters|lobsters]] and [[wikipedia:hydras|hydras]], which do not show symptoms of aging.<ref>{{cite book |author=Greg Critser |title=Eternity Soup: Inside the Quest to End Aging |url=https://books.google.com.ar/books?id=5ikIgPLoM7IC&pg=PT173&lpg=PT173&dq=The+term+negligible+senescence+is+first+used+by+professor+Caleb+Finch&source=bl&ots=8x928wNPqZ&sig=tsCM_DxFBQ-43HGdliqI1NsrsAs&hl=es&sa=X&ved=0ahUKEwjR6rLK79DMAhXCQpAKHfDdBKEQ6AEIOjAE#v=onepage&q=The%20term%20negligible%20senescence%20is%20first%20used%20by%20professor%20Caleb%20Finch&f=false |location= |publisher= |page= |date= |isbn=}}</ref> ||  
+
|1990-1995 || Scientific development || The term ''[[wikipedia:negligible senescence|negligible senescence]]'' is first used by professor [[wikipedia:Caleb Finch|Caleb Finch]] to describe organisms such as [[wikipedia:lobsters|lobsters]] and [[wikipedia:hydras|hydras]], which do not show symptoms of aging.<ref>{{cite book |author=Greg Critser |title=Eternity Soup: Inside the Quest to End Aging |url=https://books.google.com.ar/books?id=5ikIgPLoM7IC&pg=PT173&lpg=PT173&dq=The+term+negligible+senescence+is+first+used+by+professor+Caleb+Finch&source=bl&ots=8x928wNPqZ&sig=tsCM_DxFBQ-43HGdliqI1NsrsAs&hl=es&sa=X&ved=0ahUKEwjR6rLK79DMAhXCQpAKHfDdBKEQ6AEIOjAE#v=onepage&q=The%20term%20negligible%20senescence%20is%20first%20used%20by%20professor%20Caleb%20Finch&f=false |location= |publisher= |page= |date= |isbn=}}</ref> ||  
 
|-
 
|-
|1991 || Theory || [[wikipedia:Leonid A. Gavrilov|Leonid A. Gavrilov]] and Natalia S. Gavrilova apply the principles of [[wikipedia:reliability theory|reliability theory]] to human biology, proposing a ''[[wikipedia:Reliability theory of aging and longevity|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 [[wikipedia:Redundancy (engineering)|redundancy]].<ref>{{cite magazine |author= A. J. S. Rayl |title=Aging, in Theory: A Personal Pursuit |url=http://www.the-scientist.com/?articles.view/articleNo/14015/title/Aging--in-Theory--A-Personal-Pursuit/ |magazine= The Scientist|location= |publisher= |date= May 13, 2002 |access-date= }}</ref><ref>Leonid A. Gavrilov, Natalia S. Gavrilova; V.P. Skulachev (ed.); John and Liliya Payne (trans.) (1991). ''The Biology of Life Span: A Quantitative Approach''. Chur; New York: Harwood Academic Publishers. ISBN 9783718649839.</ref>||
+
|1991 || Scientific development (theory) || [[wikipedia:Leonid A. Gavrilov|Leonid A. Gavrilov]] and Natalia S. Gavrilova apply the principles of [[wikipedia:reliability theory|reliability theory]] to human biology, proposing a ''[[wikipedia:Reliability theory of aging and longevity|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 [[wikipedia:Redundancy (engineering)|redundancy]].<ref>{{cite magazine |author= A. J. S. Rayl |title=Aging, in Theory: A Personal Pursuit |url=http://www.the-scientist.com/?articles.view/articleNo/14015/title/Aging--in-Theory--A-Personal-Pursuit/ |magazine= The Scientist|location= |publisher= |date= May 13, 2002 |access-date= }}</ref><ref>Leonid A. Gavrilov, Natalia S. Gavrilova; V.P. Skulachev (ed.); John and Liliya Payne (trans.) (1991). ''The Biology of Life Span: A Quantitative Approach''. Chur; New York: Harwood Academic Publishers. ISBN 9783718649839.</ref>||
 
|-
 
|-
|  1993 || Discovery ||Dr. [[wikipedia:Cynthia Kenyon|Cynthia Kenyon]] discovers that a single-gene mutation ([[wikipedia:Daf-2|Daf-2]]) can double the lifespan of  nematode ''[[wikipedia:Caenorhabditis elegans|Caenorhabditis elegans]]'' and that this can be reversed by a second mutation in [[wikipedia:daf-16|daf-16]]m.<ref>{{cite web|url=http://www.sfgate.com/magazine/article/Finding-the-Fountain-of-Youth-Where-will-UCSF-2667274.php|title= Finding the Fountain of Youth / Where will UCSF biochemist Cynthia Kenyon's age-bending experiments with worms lead us?}}</ref><ref>{{cite journal |vauthors=Kenyon C, Chang J, Gensch E, Rudner A, Tabtiang R | title=A C. elegans mutant that lives twice as long as wild type | journal=[[wikipedia:Nature (journal)|Nature]] | volume=366 | issue=6454 | year=1993 | pages=461–464 | pmid=8247153 | doi=10.1038/366461a0}}</ref> ||
+
|  1993 || Scientific development ||Dr. [[wikipedia:Cynthia Kenyon|Cynthia Kenyon]] discovers that a single-gene mutation ([[wikipedia:Daf-2|Daf-2]]) can double the lifespan of  nematode ''[[wikipedia:Caenorhabditis elegans|Caenorhabditis elegans]]'' and that this can be reversed by a second mutation in [[wikipedia:daf-16|daf-16]]m.<ref>{{cite web|url=http://www.sfgate.com/magazine/article/Finding-the-Fountain-of-Youth-Where-will-UCSF-2667274.php|title= Finding the Fountain of Youth / Where will UCSF biochemist Cynthia Kenyon's age-bending experiments with worms lead us?}}</ref><ref>{{cite journal |vauthors=Kenyon C, Chang J, Gensch E, Rudner A, Tabtiang R | title=A C. elegans mutant that lives twice as long as wild type | journal=[[wikipedia:Nature (journal)|Nature]] | volume=366 | issue=6454 | year=1993 | pages=461–464 | pmid=8247153 | doi=10.1038/366461a0}}</ref> ||
 
|-
 
|-
 
|1994||Book||[[wikipedia:Leonard Hayflick|Leonard Hayflick]] publishes ''How and Why we Age''.<ref>{{cite web|url=https://repository.asu.edu/attachments/163946/content/Bartlett_asu_0010N_15494.pdf|title=A History of Cellular Senescence and Its Relation to Stem Cells in the Twentieth and Twenty-First Centuries  |author=Zane Bartlett |date=|accessdate=4 August 2016}}</ref>||
 
|1994||Book||[[wikipedia:Leonard Hayflick|Leonard Hayflick]] publishes ''How and Why we Age''.<ref>{{cite web|url=https://repository.asu.edu/attachments/163946/content/Bartlett_asu_0010N_15494.pdf|title=A History of Cellular Senescence and Its Relation to Stem Cells in the Twentieth and Twenty-First Centuries  |author=Zane Bartlett |date=|accessdate=4 August 2016}}</ref>||
 
|-
 
|-
|1995||Development||Detection of [[wikipedia:senescent cell|senescent cell]]s using a [[wikipedia:cytochemical assay|cytochemical assay]] is first described.<ref>{{cite web|title=Senescence Associated β-galactosidase Staining|url=http://www.bio-protocol.org/e247|accessdate=20 August 2016}}</ref>||  
+
| 1995 || Scientific development || Detection of [[wikipedia:senescent cell|senescent cell]]s using a [[wikipedia:cytochemical assay|cytochemical assay]] is first described.<ref>{{cite web|title=Senescence Associated β-galactosidase Staining|url=http://www.bio-protocol.org/e247|accessdate=20 August 2016}}</ref> ||  
 
|-
 
|-
|2003|| Organization || Dr. [[wikipedia:Aubrey de Grey|Aubrey de Grey]] and [[wikipedia:David Gobel|David Gobel]] form the [[wikipedia:Methuselah Foundation|Methuselah Foundation]], which gives financial grants to anti-aging research projects.<ref>[http://mfoundation.org/about Methuselah Foundation - About]</ref> || [[wikipedia:Springfield, Virginia|Springfield, Virginia]], U.S.A.
+
|2003|| Organization || Dr. [[wikipedia:Aubrey de Grey|Aubrey de Grey]] and [[wikipedia:David Gobel|David Gobel]] form the [[wikipedia:Methuselah Foundation|Methuselah Foundation]], which gives financial grants to anti-aging research projects.<ref>[http://mfoundation.org/about Methuselah Foundation - About]</ref> || {{w|United States}} ([[wikipedia:Springfield, Virginia|Springfield, Virginia]])
 
|-
 
|-
|2009|| Organization || De Grey and several others found the [[wikipedia:SENS Research Foundation|SENS Research Foundation]] with aims at conducting research into aging and funding other anti-aging research projects at various universities.<ref>Ben Best (2013) [http://www.lef.org/magazine/mag2013/jul2013_Interview-with-Aubrey-de-Grey-PhD_01.htm "Interview with Aubrey de Grey, PhD"]. ''Life Extension Magazine''.</ref><ref>{{Cite news|title = Jason Hope|date = December 9, 2010 |publisher = Internet Entrepreneur Pledges A Donation To SENS Foundation - JasonHope.com|url = http://jasonhope.com/press/61-sens-foundation}}</ref><ref>[http://sens.org/files/pdf/2011_Research_Report.pdf research report 2011]. Sens Foundation</ref> ||[[wikipedia:Mountain View, California|Mountain View, California]], U.S.A
+
|2009|| Organization || {{w|Aubrey de Grey}} and several others found the [[wikipedia:SENS Research Foundation|SENS Research Foundation]] with aims at conducting research into aging and funding other anti-aging research projects at various universities.<ref>Ben Best (2013) [http://www.lef.org/magazine/mag2013/jul2013_Interview-with-Aubrey-de-Grey-PhD_01.htm "Interview with Aubrey de Grey, PhD"]. ''Life Extension Magazine''.</ref><ref>{{Cite news|title = Jason Hope|date = December 9, 2010 |publisher = Internet Entrepreneur Pledges A Donation To SENS Foundation - JasonHope.com|url = http://jasonhope.com/press/61-sens-foundation}}</ref><ref>[http://sens.org/files/pdf/2011_Research_Report.pdf research report 2011]. Sens Foundation</ref> || {{w|United States}} ([[wikipedia:Mountain View, California|Mountain View, California]])
 
|-
 
|-
| 2010 || Achievement||[[wikipedia:Harvard university|Harvard]] scientists reverse aging process in mice through reactivation of [[wikipedia:telomerase|telomerase]].<ref>{{cite web|url=https://www.theguardian.com/science/2010/nov/28/scientists-reverse-ageing-mice-humans |title=Harvard scientists reverse the ageing process in mice – now for humans }}</ref>||U.S.A.
+
| 2010 || Scientific development ||[[wikipedia:Harvard university|Harvard]] scientists reverse aging process in mice through reactivation of [[wikipedia:telomerase|telomerase]].<ref>{{cite web|url=https://www.theguardian.com/science/2010/nov/28/scientists-reverse-ageing-mice-humans |title=Harvard scientists reverse the ageing process in mice – now for humans }}</ref>|| {{w|United States}}
 
|-
 
|-
|2013|| Organization || [[wikipedia:Google|Google]] announces [[wikipedia:Calico (company)|Calico]], with the purpose of harnessing new technologies to increase scientific understanding of the biology of aging.<ref>{{cite web|url=http://www.cnn.com/2013/10/03/tech/innovation/google-calico-aging-death/|title=How Google's Calico aims to fight aging and 'solve death'|author=Arion McNicoll, Arion |date=3 October 2013|work=CNN}}</ref> ||[[wikipedia:San Francisco|San Francisco]], U.S.A
+
|2013|| Organization || [[wikipedia:Google|Google]] announces [[wikipedia:Calico (company)|Calico]], with the purpose of harnessing new technologies to increase scientific understanding of the biology of aging.<ref>{{cite web|url=http://www.cnn.com/2013/10/03/tech/innovation/google-calico-aging-death/|title=How Google's Calico aims to fight aging and 'solve death'|author=Arion McNicoll, Arion |date=3 October 2013|work=CNN}}</ref> || {{w|United States}} ([[wikipedia:San Francisco|San Francisco]])
 
|-
 
|-
| 2016 || Discovery || Scientists demonstrate for the first time that [[wikipedia:mitochondria|mitochondria]] are major triggers of cell aging.<ref>{{cite journal |author=Clara Correia‐Melo, Francisco DM Marques, Rhys Anderson, Graeme Hewitt, Rachael Hewitt, John Cole, Bernadette M Carroll, Satomi Miwa, Jodie Birch, Alina Merz, Michael D Rushton, Michelle Charles, Diana Jurk, Stephen WG Tait, Rafal Czapiewski, Laura Greaves, Glyn Nelson, Mohammad Bohlooly‐Y, Sergio Rodriguez‐Cuenca, Antonio Vidal‐Puig, Derek Mann, Gabriele Saretzki, Giovanni Quarato, Douglas R Green, Peter D Adams, Thomas von Zglinicki, Viktor I Korolchuk, João F Passos |date= |title=Mitochondria are required for pro‐ageing features of the senescent phenotype |url=http://emboj.embopress.org/content/35/7/724 |journal=The EMBO Journal |publisher= |volume= 35|issue= |pages= 724–742|doi=10.15252/embj.201592862 |pmc= |pmid= 26848154 |year=2016}}</ref><ref>{{cite web|url=http://www.ncl.ac.uk/press/news/2016/02/mitochondriashowntotriggercellageing/|title=Mitochondria shown to trigger cell ageing}}</ref>|| [[wikipedia:Newcastle upon Tyne|Newcastle upon Tyne]], UK ([[wikipedia:Newcastle University|Newcastle University]])
+
| 2016 || Scientific development || Scientists demonstrate for the first time that [[wikipedia:mitochondria|mitochondria]] are major triggers of cell aging.<ref>{{cite journal |author=Clara Correia‐Melo, Francisco DM Marques, Rhys Anderson, Graeme Hewitt, Rachael Hewitt, John Cole, Bernadette M Carroll, Satomi Miwa, Jodie Birch, Alina Merz, Michael D Rushton, Michelle Charles, Diana Jurk, Stephen WG Tait, Rafal Czapiewski, Laura Greaves, Glyn Nelson, Mohammad Bohlooly‐Y, Sergio Rodriguez‐Cuenca, Antonio Vidal‐Puig, Derek Mann, Gabriele Saretzki, Giovanni Quarato, Douglas R Green, Peter D Adams, Thomas von Zglinicki, Viktor I Korolchuk, João F Passos |date= |title=Mitochondria are required for pro‐ageing features of the senescent phenotype |url=http://emboj.embopress.org/content/35/7/724 |journal=The EMBO Journal |publisher= |volume= 35|issue= |pages= 724–742|doi=10.15252/embj.201592862 |pmc= |pmid= 26848154 |year=2016}}</ref><ref>{{cite web|url=http://www.ncl.ac.uk/press/news/2016/02/mitochondriashowntotriggercellageing/|title=Mitochondria shown to trigger cell ageing}}</ref>|| {{w|United Kingdom}} ([[wikipedia:Newcastle University|Newcastle University]])
 +
|-
 +
| 2017 (December) || Scientific development || Study shows that preventing {{w|wrinkle}}s could be as easy as expressing a protein called {{w|FKBP1b}}.<ref>{{cite web|title=Fasting can delay the signs of AGING, claims researcher following an array of 'promising' trials into the controversial fad of restricting calories  Read more: http://www.dailymail.co.uk/health/article-5199019/Restricting-calories-delay-aging-says-researcher.html#ixzz536ekY47y  Follow us: @MailOnline on Twitter | DailyMail on Facebook|url=http://www.dailymail.co.uk/health/article-5199019/Restricting-calories-delay-aging-says-researcher.html|website=dailymail.co.uk|accessdate=3 January 2018}}</ref> ||
 +
|-
 +
| 2018 (January) || Scientific development || Researchers at the {{w|University of Texas Health Science Center}} (UTHealth) in {{w|Houston}} report a connection between accelerated epigenetic aging and bipolar disorder. The results could explain why people suffering from bipolar disorder are more likely to die from age-related diseases.<ref>{{cite web|title=Bipolar Disorder Linked to Accelerated Epigenetic Aging|url=https://www.whatisepigenetics.com/bipolar-disorder-linked-accelerated-epigenetic-aging/|website=whatisepigenetics.com|accessdate=3 January 2018}}</ref>
 
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==Meta information on the timeline==
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===How the timeline was built===
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The initial version of the timeline was written by [[User:Sebastian]].
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{{funding info}} is available.
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===What the timeline is still missing===
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[https://www.cnbc.com/2017/10/20/science-diet-fasting-may-be-more-important-than-just-eating-less.html]
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[http://bigthink.com/21st-century-spirituality/how-the-mind-body-connection-determines-how-you-age?utm_campaign=Echobox&utm_medium=Social&utm_source=Facebook]
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[https://m.phys.org/news/2017-10-mathematically-impossible-aging-scientists.html]
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[http://www.smh.com.au/technology/sci-tech/three-australian-teams-race-each-other-and-time-itself-to-crack-a-cure-for-aging-20171027-gz9j2g.html]
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===Timeline update strategy===
  
 
==See also==
 
==See also==
  
 
* [[wikipedia:Timeline of Alzheimer's disease|Timeline of Alzheimer's disease]]
 
* [[wikipedia:Timeline of Alzheimer's disease|Timeline of Alzheimer's disease]]
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==External links==
  
 
==References==
 
==References==
  
{{reflist|30em}}
+
{{Reflist|30em}}
  
 
[[wikipedia:Category:Senescence|Category:Senescence]]
 
[[wikipedia:Category:Senescence|Category:Senescence]]
 
[[wikipedia:Category:Medicine timelines|Category:Medicine timelines]]
 
[[wikipedia:Category:Medicine timelines|Category:Medicine timelines]]

Latest revision as of 00:59, 3 January 2018

The content on this page is forked from the English Wikipedia page entitled "Timeline of senescence research". The original page still exists at Timeline of senescence research. The original content was released under the Creative Commons Attribution/Share-Alike License (CC-BY-SA), so this page inherits this license.

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.

Big picture

Year/period Event
Ancient Greece Early speculations on aging are focussed on the bodily humoral imbalance and on the gradual loss of inner heat.[1]
Middle Age/Renaissance Rejuvenating or stopping the aging process is a major concern in this period.[1]
Renaissance–18th century Some themes around which aging and senescence research revolves around are the idea that senescence is itself an illness, the image of the aged body as a lamp in which life-fuel has run out, the character alterations of elders, and the attempt to prolong life through specific diet or by substituting damaged body parts.[1]
Late 19th–20th century Starting from the so-called "fin-de-siècle" period, scientific optimism flourishes, and life-extensionism represents the most radical form of the trend.[2] Life expectancy starts to rise in the Western world.[3]
20th century Senescence research focuses on four major directions: cellular theories, immune-metabolic models, evolutionary explanations and molecular biology-based approaches.[1]

Modern anti-aging organizations merge and their proliferation multiplies toward the 2000s.[2]

Full timeline

Year/period Type of Event Event Location
c. 99 BC – c. 55 BC Scientific development (theory) Roman 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.[4]
5th century Scientific development (theory) Early 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.[1] Greece
1825 Scientific development Benjamin Gompertz proposes an exponential increase in death rates with age, giving birth to what later will be called The Gompertz-Makeham law [5][6][7]
1891 Scientific development (theory) August 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.[8][9]
1908 Scientific development (theory) Max 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.[10][11]
1913 Organization The Life Extension Institute is inaugurated as a longevity research center, with US president William Howard Taft as chairman.[12][2] United States
1928 Scientific development (theory) Raymond 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.[13]
1934 Scientific development (theory) Mary Crowell and Clive McCay of Cornell University discover that calorie restriction can extend lifespan twofold in rats.[14]
1945–1949 Scientific development The advent of molecular biology changes the theoretical perception of aging dramatically, as the precise molecular structure of proteins and genetic material becomes known.[2] United States
1950s Scientific development (theory) Denham 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.[13]
1952 Scientific development (theory) Peter 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.[4]
1957 Scientific development (theory) George 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.[4][15]
1958 Scientific development (theory) G. 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.[2]
1961 Scientific development (theory) American 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.[16][17][18] Philadelphia
1965–1969 Scientific development The strong effect of age on DNA methylation levels is discovered,[19] thus rendering it an accurate biological clock in humans and chimpanzees.[20]
1967 Scientific development (theory) C. 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.[21] This theory becomes stronger through further experimental support during the following decades.[22][23]
1969 Publication American physician Roy Walford publishes The Immunologic Theory of Aging, contributing to the basis for many current ideas about immunological aging.[24]
1974 Organization The National Institute on Aging (NIA) is formed as a division of the United States 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.[25][26] United States (Baltimore)
1975–1984 Scientific development Elizabeth Blackburn discovers the unusual nature of telomeres, with their simple repeated DNA sequences composing chromosome ends.[27][28] 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.[29] Further experiments establish the role of telomere shortening in cellular aging and telomerase reactivation in cell immortalization.[30]
1977 Scientific development (theory) Thomas 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.[31]
1990 Organization The 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.[32][33] United States (UCLA)
1990-1995 Scientific development The 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.[34]
1991 Scientific development (theory) Leonid 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.[35][36]
1993 Scientific development Dr. Cynthia 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.[37][38]
1994 Book Leonard Hayflick publishes How and Why we Age.[39]
1995 Scientific development Detection of senescent cells using a cytochemical assay is first described.[40]
2003 Organization Dr. Aubrey de Grey and David Gobel form the Methuselah Foundation, which gives financial grants to anti-aging research projects.[41] United States (Springfield, Virginia)
2009 Organization Aubrey de 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.[42][43][44] United States (Mountain View, California)
2010 Scientific development Harvard scientists reverse aging process in mice through reactivation of telomerase.[45] United States
2013 Organization Google announces Calico, with the purpose of harnessing new technologies to increase scientific understanding of the biology of aging.[46] United States (San Francisco)
2016 Scientific development Scientists demonstrate for the first time that mitochondria are major triggers of cell aging.[47][48] United Kingdom (Newcastle University)
2017 (December) Scientific development Study shows that preventing wrinkles could be as easy as expressing a protein called FKBP1b.[49]
2018 (January) Scientific development Researchers at the University of Texas Health Science Center (UTHealth) in Houston report a connection between accelerated epigenetic aging and bipolar disorder. The results could explain why people suffering from bipolar disorder are more likely to die from age-related diseases.[50]

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How the timeline was built

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Funding information for this timeline is available.

What the timeline is still missing

[1] [2] [3] [4]

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See also

External links

References

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  4. 4.0 4.1 4.2 Daniel Fabian; Thomas Flatt. "The Evolution of Aging". Nature. 
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  25. Ofahengaue Vakalahi, Halaevalu F.; Simpson, Gaynell M.; Giunta, Nancy. The Collective Spirit of Aging Across Cultures. p. 20. Retrieved 21 December 2016. 
  26. "National Institute of Aging". 
  27. "ELIZABETH BLACKBURN: TELOMERES AND TELOMERASE". 
  28. Blackburn AM; Gall, Joseph G. (March 1978). "A tandemly repeated sequence at the termini of the extrachromosomal ribosomal RNA genes in Tetrahymena". J. Mol. Biol. 120 (1): 33–53. PMID 642006. doi:10.1016/0022-2836(78)90294-2. 
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  32. Nuwer, Rachel (4 July 2014). "Keeping Track of the Oldest People in the World". Smithsonion.com. Retrieved 3 January 2015. 
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  34. Greg Critser. Eternity Soup: Inside the Quest to End Aging. 
  35. A. J. S. Rayl (May 13, 2002). "Aging, in Theory: A Personal Pursuit". The Scientist. 
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  37. "Finding the Fountain of Youth / Where will UCSF biochemist Cynthia Kenyon's age-bending experiments with worms lead us?". 
  38. Kenyon C, Chang J, Gensch E, Rudner A, Tabtiang R (1993). "A C. elegans mutant that lives twice as long as wild type". Nature. 366 (6454): 461–464. PMID 8247153. doi:10.1038/366461a0. 
  39. Zane Bartlett. "A History of Cellular Senescence and Its Relation to Stem Cells in the Twentieth and Twenty-First Centuries" (PDF). Retrieved 4 August 2016. 
  40. "Senescence Associated β-galactosidase Staining". Retrieved 20 August 2016. 
  41. Methuselah Foundation - About
  42. Ben Best (2013) "Interview with Aubrey de Grey, PhD". Life Extension Magazine.
  43. "Jason Hope". Internet Entrepreneur Pledges A Donation To SENS Foundation - JasonHope.com. December 9, 2010. 
  44. research report 2011. Sens Foundation
  45. "Harvard scientists reverse the ageing process in mice – now for humans". 
  46. Arion McNicoll, Arion (3 October 2013). "How Google's Calico aims to fight aging and 'solve death'". CNN. 
  47. Clara Correia‐Melo, Francisco DM Marques, Rhys Anderson, Graeme Hewitt, Rachael Hewitt, John Cole, Bernadette M Carroll, Satomi Miwa, Jodie Birch, Alina Merz, Michael D Rushton, Michelle Charles, Diana Jurk, Stephen WG Tait, Rafal Czapiewski, Laura Greaves, Glyn Nelson, Mohammad Bohlooly‐Y, Sergio Rodriguez‐Cuenca, Antonio Vidal‐Puig, Derek Mann, Gabriele Saretzki, Giovanni Quarato, Douglas R Green, Peter D Adams, Thomas von Zglinicki, Viktor I Korolchuk, João F Passos (2016). "Mitochondria are required for pro‐ageing features of the senescent phenotype". The EMBO Journal. 35: 724–742. PMID 26848154. doi:10.15252/embj.201592862. 
  48. "Mitochondria shown to trigger cell ageing". 
  49. "Fasting can delay the signs of AGING, claims researcher following an array of 'promising' trials into the controversial fad of restricting calories Read more: http://www.dailymail.co.uk/health/article-5199019/Restricting-calories-delay-aging-says-researcher.html#ixzz536ekY47y Follow us: @MailOnline on Twitter". dailymail.co.uk. Retrieved 3 January 2018.  Text " DailyMail on Facebook" ignored (help); External link in |title= (help)
  50. "Bipolar Disorder Linked to Accelerated Epigenetic Aging". whatisepigenetics.com. Retrieved 3 January 2018. 

Category:Senescence Category:Medicine timelines