Difference between revisions of "Timeline of senescence research"

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| 1990-1995 || Scientific development || Concept introduction || The term ''{{w|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 || Concept introduction || The term ''{{w|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> ||  
 
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| 1991 || || || Applying a similar approach by Nesse in 1988, but to a larger set of wild mammalian populations, Promislow again concludes that there is detectable senescence in wild populations of animals.<ref name="Shefferson"/> ||
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| 1991 || Scientific development || [[w:Category:Theories of biological aging|Theory]] || {{w|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 || [[w:Category:Theories of biological aging|Theory]] || {{w|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>||
 
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Revision as of 18:56, 8 November 2021

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 is defined as "the process of physiological or biological decay leading to increasing mortality rates and/or decreasing fertility rates with age". This should be distinguished from "aging", which can be viewed simply as the march of time, with no physiological decay implied.

Sample questions

The following are some interesting questions that can be answered by reading this timeline:

  • What are some of the numerous theories of aging having been proposed throughout history?
    • Sort the full timeline by "Research type (when applicable)" and look for the group of rows with value "Theory".
  • What are some significant studies on senescence conducted in research labs?
    • Sort the full timeline by "Research type (when applicable)" and look for the group of rows with value "Laboratory".
  • What are some notable publications specialized in the field of senescence?
    • Sort the full timeline by "Event type" and look for the group of rows with value "Literature".
    • You will see some publications by Leonard Hayflick, Roy Halford and Aubrey de Grey.
    • For specialized jornals, sort the full timeline by "Event type" and look for the group of rows with value "Literature (journal)"
  • What are some notable concepts having been introduced in the field of senescence?
    • Sort the full timeline by "Research type (when applicable)" and look for the group of rows with value "Concept introduction".
    • You will see descriptions around concepts like gerontology, senescence, and programmed cell-death.

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 revolve 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]
19th century The modern evolutionary theory of senescence is rooted in the late century.[2] Starting from the so-called "fin-de-siècle period, scientific optimism flourishes, and life-extensionism represents the most radical form of the trend.[3] Life expectancy starts to rise in the Western world.[4]
20th century Since the 1930s, it is understood that restricting calories can extend lifespan in laboratory animals.[5] After the Second World War, modern knowledge accumulates. The 1950s see the first attempts to distinguish, measure and compare the functional and chronological ages of individuals, of which biological considerations were an important component.[6][7] The beginning of the term “senescence” in the context of mammalian cell cultures begins in the 1960s with the work of Hayflick and Moorhead.[8] Also by this same decade, biologists start becoming aware of mortality leveling-off.[9] Around the start of the 1970s, senescence research starts broadening its evolutionary scope.[2] During the mid-1970s, there is considerable interest in the idea that cells might become destabilized and thereby precipitates onto a pathway of progressive deterioration.[2] In the 1980s, the field of life-span psychology is born.[10] In the 1990s, Caleb Finch gives serious consideration to organisms that exhibit negligible senescence and experience no, or only very small, increases in mortality rate with age.[2]
21st century Modern anti-aging organizations merge and their proliferation multiplies toward the 2000s.[3] In the 21st century, research activity increases, as well as interdisciplinary collaboration of senescence research with other fields, such as data science. In the second half of 2010s official discussions about the possibility of recognizing aging as a disease emmerge.[11][12][13][14][15]

Visual and numerical data

Mentions on Google Scholar

The table below summarizes per-year mentions of senescence–related topics (entries without quotation marks) on Google Scholar as of May 13, 2021.

Year Senescence Aging Longevity Life extension
1980 2,840 24,300 7,200 48,900
1985 3,760 36,300 9,210 43,400
1990 5,840 69,200 13,400 101,000
1995 8,150 114,000 18,300 131,000
2000 12,200 237,000 33,600 269,000
2002 13,400 302,000 41,600 299,000
2004 16,600 403,000 51,300 296,000
2006 21,500 470,000 62,900 341,000
2008 26,800 481,000 74,500 364,000
2010 33,500 587,000 85,400 397,000
2012 43,500 712,000 109,000 409,000
2014 47,900 653,000 103,000 366,000
2016 47,200 466,000 88,800 298,000
2017 45,300 441,000 81,500 254,000
2018 43,800 297,000 74,600 194,000
2019 39,500 201,000 59,400 148,000
2020 34,800 130,000 44,200 103,000
Senescence research.png

Google Trends

The comparative chart below shows Google Trends data for Senescence (Topic), Cellular senescence (Topic) and Negligible senescence (Topic), from January 2004 to April 021, when the screenshot was taken. Interest is also ranked by country and displayed on world map.[16]

Senescence research gt.png

Google Ngram Viewer

The chart below shows Google Ngram Viewer data for Senescence research, from 1950 to 2019.[17]

Senescence research ngram.png

Wikipedia Views

The chart below shows pageviews of the English Wikipedia article Senescence, on desktop from December 2007, and on mobile-web, desktop-spider, mobile-web-spider and mobile app, from July 2015; to March 2021.[18]

Senescence wv.png

Full timeline

Year/period Type of Event Research type (when applicable) Event Location
c. 99 BC – c. 55 BC Scientific development 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.[19]
Lucretius1.png
5th century Scientific development 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
Hippocrates.jpg
1825 Scientific development British mathematician Benjamin Gompertz proposes an exponential increase in death rates with age, giving birth to what later will be called The Gompertz-Makeham law.[20][21] The simplest form of the law is: p = a + bx. According to the law, the probability of death p is defined as the sum of age-independent component a and the component depending of age bx which with age increases exponentially. If we place organisms in an absolutely protected environment and in this way make the first component negligible, the probability of death will be completely defined by the second component which actually describes the probability to die from aging. United Kingdom
Gompertz.png
1882 Scientific development Theory German evolutionary biologist August Weismann introduces the wear and tear theory of aging, which sustains that cells and tissues have vital parts that wear out resulting in aging. "Like components of an aging car, parts of the body eventually wear out from repeated use, killing them and then the body."[5] Germany
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.[22][23] Germany
August Weismann.jpg
1903 Scientific development Concept introduction Russian zoologist Ilya Mechnikov coins the term "gerontology".[24][25][26]
1904 Scientific development Theory Metchnikoff introduces the Autointoxication theory of aging, which is considered important at the whole animal level.[27] This is one of the first toxic theories as Metchnikoffs proposes the idea of autointoxication by products of bacterial origin, primarily from bacterial processes in the large intestine. Metchnikoff believes that even simple changes of acidity by the consumption of yogurt could inhibit the production of bacterial toxins.[28]
1908 Scientific development Theory German physiologist 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.[29][30] Some studies conclude that the rate‐of‐living theory does not hold true for terrestrial vertebrates, and suggest that life expectancy is driven by selection arising from extrinsic mortality factors.[31] Support for this theory is bolstered by studies linking a lower basal metabolic rate (evident with a lowered heartbeat) to increased life expectancy.[32][33] However, in a 2007 analysis it would be shown that, when modern statistical methods for correcting for the effects of body size and phylogeny are employed, metabolic rate does not correlate with longevity in mammals or birds.[34] Germany
Max Rubner.jpg
1928 Scientific development Theory American biologist 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.[35] Further studies would demonstrate that rats kept on restricted diets and in cold environments live longer and that these conditions have the appearance and behavior of younger animals.[36] United States
Dr. Raymond Pearl, Food. Adm. LCCN2016824384 (cropped).jpg
1930 Literature (journal) The first world's journal about aging and longevity is established in Japan.It's titled Acta Gerontologica Japonica (Yokufuen Chosa Kenkyu Kiyo).[37] Japan
1934 Scientific development Laboratory Mary Crowell and Clive McCay at Cornell University discover that calorie restriction can extend lifespan twofold in rats.[38] United States
1938 Organization The German Society for Aging Research (German: Deutsche Gesellschaft für Altersforschung) is founded in Leipzig as the first specialized society dedicated to the study of aging. The founder, Max Bürger, also establishes the specialized journal Zeitschrift für Altersforschung , which becomes the third such journal in the world after the previously mentioned Japanese and Romanian journals.[39] Germany
1938 Conference The world's first scientific conference on aging and longevity is held in Kiev.[40][41] Ukraine (USSR at the time)
1939 Organization (non-profit) The British Society for Research on Aging is founded by Russian-British gerontologist Vladimir Korenchevsky.[42] It promotes research to understand the causes and effects of the aging process.[43] United Kingdom
Vladimir Korenchevsky
1940 Scientific development Theory Nagorny introduces a theory of aging based on age changes, which is described as the stabilization and inactivation (insolubilization) of intercellular structural proteins. Nagorny postulates that aging is linked to the accumulation of intercellular inactivated "metaplasmic" proteins due to the inability of enzymes to destroy them.[28]
1942 Scientific development Theory Johan Björkstein proposes the cross‐linkage theory of aging. According to it, aging results from the accumulation of intra‐ and intermolecular covalent bonds between molecules, termed “cross‐links.”[44][5] Recent studies show that cross-linking reactions are involved in the age related changes in the studied proteins.[45]
1945 Scientific development Theory The idea that free radicals are toxic agents is first proposed by Argentinian biologist Rebeca Gerschman and colleagues.[46]
1945 Organization The Gerontological Society of America is founded "to promote the scientific study of aging, to encourage exchanges among researchers and practitioners from the various disciplines related to gerontology, and to foster the use of gerontological research in forming public policy".[47] United States
1945–1949 Scientific development Laboratory The advent of molecular biology changes the theoretical perception of aging dramatically, as the precise molecular structure of proteins and genetic material becomes known.[3] United States
1946 Literature (journal) The Journal of Gerontology is founded.[48] United States
1947 Scientific development Theory Bogomolets links aging with the functional deterioration of connective tissues.[28]
1950 Organization The International Association of Gerontology is formed.[49]
1952 Scientific development Theory British biologist Peter Medawar formulates the first modern theory of mammal aging, known as Mutation accumulation theory, whereby the mechanism of action involves random, detrimental germline mutations of a kind that happen to show their effect only late in life.[19]
Peter Brian Medawar.jpg
1954 Scientific development Theory Soviet scientist Vladimir Dilman formulates the elevation hypothesis of aging, a hypothesis known only in the USSR at first. Later, in 1968, it would take the form and became known as the neuroendocrine theory of aging.[50][51][52] Russia (USSR at the time)
1954 Scientific development Theory The Free-radical theory of aging (first introduced by Dr. Rebeca Gerschman) is developed by Dr. Denham Harman, this theory proposes that superoxide and other free radicals cause damage to the macromolecular components of the cell, giving rise to accumulated damage causing cells, and eventually organs, to stop functioning.[5]
1954 Scientific development Theory Research by Nikitin introduces a theory of aging based on age changes, and described as the accumulation of protein-DNA cross-links and progressive stabilization of chromatin complexes. This theory is further elaborated by von Hahn.[28]
1956 Scientific development Theory American chemist Denham Harman presents the free radical theory of aging, which states that organisms age over time due to the accumulation of damage from free radicals in the body.[35] Harman is known as the "father of the free radical theory of aging".[53][54] Today, an increasing number of studies contradict this theory.[55] United States
1956 Scientific development Theory Benefitted by the cosolidation of knowledge of the toxic intermediate products of normal metabolism, Vladimir Korenchevsky introduces a general toxic theory of aging.[28]
1957 Scientific development Theory American evolutionary biologist 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.[19][56] This theory extends the argument by Peter Medawar.[2] United States
1957 Scientific development Theory M. F. Sinex publishes article titled Aging and the lability of irreplacable molecules, establishing a theory based on quantitative changes of proteins, and describing as the loss of irreplaceable molecules or enzymes.[28][57]
1958 Scientific development Theory American physicists Gioacchino Failla and Leo Szilard 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.[3] United States
Gioacchino Failla
1958 Scientific development Clinical study The Baltimore Longitudinal Study of Aging begins in the United States as a clinical research program on human aging. As of 2020, it is the longest-running study of aging in that country. It consists in volunteers of different ages in healthy conditions being follow-up visited for years. Participants are tested and evaluated for many physical elements as well as for brain function, mood, personality, and social aspects of life. This program would contribute more than any other research project to the understanding of aging.[58] United States
1959 Scientific development Theory Sacher introduces a size-lifespan correlation theory, positively correlating body weight with the longevity in mammals.[28]
1959 Scientific development Theory Roy Walford proposes the Immunological theory of aging,[59] which asserts that the process of human aging is largely controlled by the immune system, which weakens as an organism ages. This makes the organism unable to fight infections and less able to destroy old and neoplastic cells. This leads to aging and will eventually lead to death.[60] United States
1961 Scientific development Concept introduction The beginning of the term “senescence” in the context of mammalian cell cultures is considered to be born out of the discovery by American anatomist Leonard Hayflick and his colleague Paul Moorhead, who describe that primary cells have a finite lifespan when cultured in vitro, contrasting cancer cells that divide without limits.[8] 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.[61][62][63] United States
1961 Scientific development Theory Vladimir Korenchevsky introduces the Endocrine theory of aging, which is considered a major theory at the organ level.[27]
1962 Scientific development Theory Romanian scientists Constantin Ion Parhon and Simion Oeriu introduce a theory of aging based on age changes, and described as the progressive demethylation of proteins.[28] Romania
Constantin Ion Parhon
1963 Scientific development Theory Leslie Orgel proposes the Error Catastrophe Theory of Aging, which is based on changes in protein biosynthesis (translation).[28] This theory states that aging is the result of the accumulation of errors in cellular molecules that are essential for cellular function and reproduction that eventually reaches a catastrophic level that is incompatible with cellular survival.[64][65]
1963 Scientific development Laboratory South African biologist Sydney Brenner suggests the ability to easily and cheaply grow large quantities of worms in the lab as being very helpful for aging research, especially when identifying long-lived mutants caenorhabditis elegans, which have a relatively short lifespan (average approximately 17 days at 20 °C), and the lifespan is largely invariant.[66]
Sydney Brenner
1964 Scientific development Concept introduction The concept of programmed cell death is introduced by American cellular biologist Richard A. Lockshin and Carroll Williams.[67] PCD consists in any active cellular process that culminates in cell death.[68] United States
Richard A. Lockshin
1964 Scientific development Theory Romanian biochemist Simion Oeriu introduces a theory of aging based on age changes, described as accumulation of -S-S, inter- and intra- molecular bonds.[28] Romania
1964 Literature British scientist Alex Comfort publishes Ageing – the Biology of Senescence, a classic book in the field. The book summarizes the state of the evolutionary study of senescence as lacking the scientific rigor seen in other disciplines. Comfort criticizes the field for yielding a number of evolutionary theories but failing to generate sufficient data to test those theories.[2]
1965 Scientific development Theory Leonard Hayflick describes cell senescence as the process that limits the number of cell divisions normal human cells can undergo in culture. This work formulates the The Cellular Senescence Theory of aging.[69][70]
1965–1969 Scientific development Laboratory The strong effect of age on DNA methylation levels is discovered,[71] thus rendering it an accurate biological clock in humans and chimpanzees.[72]
1966 Scientific development Theory Sacher introduces the Wear and tear theory of aging, which is considered an important theory at the whole animal level.[27]
1966 Scientific development William Hamilton lays out the mathematics drawing on the ideas of George C. Williams and Peter Medawar, leading to the outcome that "senescence is an inevitable outcome of evolution".[2]
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.[73] This theory becomes stronger through further experimental support during the following decades.[74][75]
1969 Scientific development Theory American physician Roy Walford introduces the autoimmune theory of aging, which asserts that with age, the immune system tends to lose efficiency and experiences widespread dysfunction, evidenced by autoimmunity (immune reactions against one's own body proteins) and a decreased ability to respond to infection and other immune challenges.[76] It is well documented that the effectiveness of the immune system peaks at puberty and gradually declines thereafter with advance in age.[77] United States
1970 Scientific development Theory Selye introduces the Stress damage theory, which is considered an important theory of aging at the whole animal level.[27]
1970 Organization The American Aging Association is founded by Denham Harman. It is a non-profit, tax-exempt biogerontology organization of scientists and laypeople dedicated to biomedical aging studies and geroscience, with the goal of slowing the aging process to extend the healthy human lifespan while preserving and restoring functions typically lost to age-related degeneration.[78] United States
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.[79][80] United States (National Institute on Aging)
1974 Scientific development Theory Study by Arthur B. Robinson introduces a theory of aging based on age changes, and described as the progressive deamination of glutaminyl and asparaginyl residues in proteins.[81][28] United States
1975 Scientific development Theory Sacher introduces a brain size–lifespan correlation theory, suggesting that larger brains make evolutionary selection of longer lifespan necessary.[28]
1975 Scientific development Laboratory Australian-American molecular biologist Elizabeth Blackburn discovers the unusual nature of telomeres, with their simple repeated DNA sequences composing chromosome ends.[82][83] 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.[84] Further experiments establish the role of telomere shortening in cellular aging and telomerase reactivation in cell immortalization.[85] United States
Elizabeth Blackburn
1976 Scientific development Theory Cutler introduces a theory of aging based on age changes, and described as the cross-links between DNA molecules.[28]
1977 Scientific development Theory English biologist Thomas Kirkwood proposes the third mainstream theory of aging, 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.[86] Considered to be the most influential line of reasoning in gerontology, this theory states that aging is caused by accumulation of random damage, which is counteracted by repair. Repair is costly and the organism allocates exactly the needed amount of energetic resources. DST would be applied to explain why women live longer than men. Women are less disposable than men, so they need a better repair and thus live longer.[87]
1977 Scientific development Theory Research started by Kirkwood establishes an aging theory on lifespan correlations with changes at the molecular level. This theory suggests that immortal germ cells may have more comprehensive repairs and may have higher accuracy of synthesis than somatic cells.[28]
1977 Scientific development Theory Holliday and colleagues introduce the commitment theory of cellular aging, which stipulates the existence of a biological clock (pace-maker).[28]
1977 Scientific development Laboratory Klass publishes that nematode C. elegans is a good system for aging studies as he establishes a method to consistently measure lifespan, concluding that this could lead to future detailed analysis combining genetics and biochemistry. Klass also finds that altering either temperature or the amount of food results in a change in lifespan. In addition, only small effects on lifespan are observed based on parental age or parental lifespan.[66]
1977 Scientific development Theory British biologist Thomas Kirkwood first proposes the disposable soma theory of aging in a Nature review article. This theory is inspired by Leslie Orgel's Error Catastrophe Theory of Aging.[88]
1977 Literature American biologists Caleb Finch and Leonard Hayflick publish the Handbook of the Biology of Aging.[9] United States
1978 Scientific development Theory Todd introduces a size-lifespan correlation theory, positively correlating size, height and longevity among tree species. He suggests a protective role of large sizes from disease, predators, etc.[28]
1978 Scientific development Theory Soviet scientist A. N. Lobachev proposes the mitochondrial non free radical theory of aging, which suggests that the main reason of accumulation of damages in mt DNA is the fact that at certain moment of cell life, the development of mitochondria begin to conflict with the development of nucleus. This theory concludes that mitochondria appears to be the «biologic clock» of the cell and programm the duration of its life.[89][90] Russia
1978 Scientific development Laboratory For research on aging, early studies in nematode C. elegans focus on the feasibility of measuring lifespan and the use of 5-Fluoro-2′-deoxyuridine (FUDR) to maintain synchronous cultures of aged animals.[66]
1979 Vaupel et al. produce one of the earliest quantitative theories of lifelong heterogeneity. Under their model, the probability of an individual dying is described by a Gompertz equation, a sigmoid function which describes growth as being slowest at the start and end of a given time period.[2]
1979 Scientific development Theory Research by D. Gershon at Technion introduces a theory of aging based on age changes, and described as age-altered enzymes theory (age-related accumulation of conformational changes in protein leading to the inactivation of enzymes).[28] Israel
1979 Scientific development Theory Kirkwood and Holliday introduce a theory correlating lifespan with changes at the molecular level. Their hypothesis suggests higher fidelity of syntheses of macromolecules in longer-lived species and cellular clones.[28]
1980 Scientific development Theory M. S. Kanungo introduces a theory of aging based on age changes, describing it as the decrease of phosphorylation and acetylation of chromatin proteins as the cause of defects and decline in transcription.[28][91]
1980 Scientific development Theory Strehler introduces an aging theory classification that underlines the interrelation between different mechanisms of aging in an attempt to unite all these types into two "supergroups": genetically programmed aging, and aging secondary to genetic qualities (entropic increase). Strehler classification groupes theories of aging into evolutionary (selection for limited lifespan), post-reproductive failure, failure of coordinating systems, pleiotropic side effects of advantageous qualities (clonal aging, autoimmunity), informational failure (changes in proteins and DNA), structural damage or loss and accumulation of dysfunctional materials (age-pigments, inactive proteins, lytic enzymes, etc.)[28]
1982 Scientific development Theory Pashko and Schwartz propose an aging theory on lifespan correlations at the cellular level, suggesting a correlation between lifespan and species-specific activity of detoxification enzymes (longer-lived animals have higher efficiency of detoxification and are more resistant to environmental toxins).[28]
1986 Organization (non-profit) The Alliance for Aging Research is founded a non-profit organization, with the purpose to promote medical and behavioral research into the aging process.[92] United States
1986 Scientific development Theory The Reliability theory of aging and longevity is proposed by Leonid Gavrilov and Natalia Gavrilova.[93][94][95][96]
1987 Scientific development Laboratory B.M. Stanulis-Praeger determines cell death to be a primary consequence of senescence.[97] United States (Tufts University, Boston)
1988 Scientific development Laboratory Genetic work by Tom Johnson et al. on mutant C. elegans mapps all of them to a single genetic locus, named age-1. This is the first breakthrough in aging research for studies based on C. elegans as this study reveals that it is possible to identify mutants that altered lifespan and more importantly, individual genes can modulate lifespan.[66]
1988 In a pioneering attempt to find quantitative evidence for senescence in wild populations of animals, Nesse concludes that it does in fact occur.[2]
1989 Scientific development Theory The network theory of aging is introduced. It supports the idea that multiple connected processes contribute to the biology of aging.[98]
1990 Scientific development Theory Russian biologist Zhores Medvedev publishes review stating that there are more than 300 theories of aging and the number is increasing.[28][99]
1990 Organization The Gerontology Research Group is founded in Los Angeles by L. Stephen Coles. IT is a network of researchers from various disciplines with common interest in outer limits of aging and how to reach them in reasonably good health.[100] United States
1990-1995 Scientific development Concept introduction 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.[101]
1991 Applying a similar approach by Nesse in 1988, but to a larger set of wild mammalian populations, Promislow again concludes that there is detectable senescence in wild populations of animals.[2]
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.[102][103]
1991 Scientific development Laboratory Leonard Hayflick describes an increase in cell degeneration and debris, resembling cell death.[8] United States
1992 Scientific development Data science The National Archive of Computerized Data on Aging (NACDA) publishes in the Internet the first 28 datasets related to aging. Gradually, the number of published datasets would surpass 1600. These datasets are available to any researcher around the world at no charge, so they can search in them for new patterns. The site also provides some tools to facilitate analysis.[104] United States
1993 Scientific development Laboratory American molecular biologist 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.[105][106] United States
Cyntia Kenyon 01.JPG
1994 Literature Leonard Hayflick publishes How and Why we Age, which elaborates on the difference between biological and chronological age and then explores on how understanding of aging has changed through history.[107]
1995 Scientific development Laboratory Detection of senescent cells using a cytochemical assay is first described.[108] Researchers discover that senescent cells express a β-galactosidase activity; and describe the “senescence-associated β galactosidase” (SA-βgal) biomarker, which conveniently identifies individual senescent cells in vitro and in vivo.[109]
1995 Scientific development Laboratory The existence of senescence-associated beta-galactosidase is proposed by Dimri et al.[110] following the observation that when beta-galactosidase assays were carried out at pH 6.0, only cells in senescence state develop staining. They proposed a cytochemical assay based on production of a blue-dyed precipitate that results from the cleavage of the chromogenic substrate X-Gal, which stains blue when cleaved by galactosidase. Since then, even more specific quantitative assays were developed for its detection at pH 6.0.[111][112][113]
1995 Scientific development Theory The remodeling theory of aging is introduced.[98] It postulates that immunosenescence or 'immuno-remodelling' is a dynamic process involving both loss and gains of immune function.[114]
1995 Scientific development Laboratory Research by by E. Wang shows that cellular senescence is associated with a reduced sensitivity to cell death.[8][115]
1998 Scientific development Laboratory Scientists manage to extend, in a laboratory environment, the life of normal human cells beyond the Hayflick limit using telomerase.[116][117]
1998 Scientific development Martinez observes that Hydra appear to grow older without showing signs of senescence. This is entirely consistent with the principle that the evolution of disposability of the soma presupposes the existence of a clear germ–soma distinction.[2]
1999 Organization (research institute) The Buck Institute for Research on Aging is established as an independent biomedical research institute devoted solely to research on aging and age-related diseases.[118][119] United States
Buck logo tagline period.png
1999 Literature Aubrey de Grey publishes The Mitochondrial Free Radical Theory of Aging, which introduces the term "engineered negligible senescence".[120]
2000 Scienific development Concept introduction Sabina Sperandio and colleagues introduce the term "paraptosis". The group uses human insulin-like growth factor 1 receptor (IGF-1R) to stimulate cell death in 293T cells and mouse embryonic fibroblasts, observing distinct differences from other forms of cell death. They coin the term "paraptosis", derived from the Greek preposition para, meaning beside or related to, and apoptosis.[121][122] United States
2003 Scientific development Laboratory Scientists report first evidence that aging of nematodes is regulated via mechanistic target ofrapamycin (mTOR) signaling.[123][124][125]
2003 Scientific development Laboratory Andrzej Bartke creates a mouse that lived 1819 days (5 years without 7 days), while the maximum lifespan for this species is 1030–1070 days.[126] Translated to human standards, such longevity is equivalent to about 180 years.[127]
2004 Scientific development Vaupel et al. describe two cases: one being a species that escapes from senescence which would exhibit the lack of such decline, referred to as "negligible senescence", and a second case in which a species shows even physiological improvement with age, which may be referred to as "negative senescence".[2]
2004 Scientific development Data science GenAge launches as the first curated database of genes related to human ageing.[128] It stores data of genes commonly altered during ageing, drawn from a microarray meta-analysis study, and the LongevityMap, a database of human genetic variants associated with longevity.[129]
2005 Kirkwood discovers that unicellular organisms such as yeasts and bacteria can exhibit forms of senescence.[2]
2006 Organization (research network) Network Aging Research (Netzwerk Alternsforschung) is founded in Germany at Heidelberg University as a research network on the topic of aging. It supports researchers in multiple fields of aging, including humanists, natural- and medical scientists.[130] Germany
2006 Literature (journal) Clinical study Peer-reviewed open access medical journal Clinical Interventions in Aging is founded, covering research in gerontology.[131]
2006 Scientific development Laboratory Shinya Yamanaka and John Gurdon receive the Nobel Prize in Physiology or Medicine for their work on reprogramming mature cells into pluripotent cells.[132] Yamanaka is the first to produce induced stem cells (iSC) from somatic cells by the simultaneous action of several factors.[133][134][135]
2007 Scientific development Laboratory Researchers manage to extend mouse lifespan via deletion of insulin receptor in the brain.[123][136]
2007 Scientific development Laboratory Researchers report first evidence that a pharmacological agent (namely, metformin) at a certain dosage is capable to increase the lifespan of mice.[123][137]
2008 Scientific development Concept introduction The concept of senescence-associated secretory phenotype (SASP) is first established by Judith Campisi and her group, who first publish on the subject.[138] United States
2008 Organization The Max Planck Institute for Biology of Ageing is founded. Its overall research aim is to obtain fundamental insights into the aging process and thus to pave the way towards healthier aging in humans.[139] Germany
2009 Scientific development Laboratory A group of three laboratories initiate a study of the effects of rapamycin on the life span of mice. After administering the agent at late ages, the team discovers a significant increase in maximum life span.[54]
2009 Recognition Laboratory Elizabeth Blackburn, Carol Greider, and Jack Szostak are awarded the Nobel Prize in Physiology or Medicine "for the discovery of how chromosomes are protected by telomeres and the enzyme telomerase."[140] These researchers are aware of the implications of their research on telomerase for the biology of aging, in particular Carol Greider who would become quite active in that field.[54]
Nobel Prize 2009-Press Conference Physiology or Medicine-04.jpg
2009 Scientific development Laboratory Researchers report association of genetic variants in insulin/IGF1 signaling with human longevity.[123][141]
2010 Scientific development Laboratory Harvard scientists reverse aging process in mice through reactivation of telomerase.[142] United States
2010 Organization (research network) The European Network in Aging Studies is established.[143][144] Europe
2012 Scientific development Laboratory Researchers from the Institute of Molecular Oncology (IFOM) in Milan and Molecular Genetics of the National Research Council (IGM-CNR) in Pavia identify for the first time a class of non-coding RNAs, called “DNA Damage Response RNAs (DDRNAs)”, laying the foundation for the future advances in cellular aging.[145] Italy
2012 Scientific development Laboratory Research by Nelson et al. shows that the bystander effect of senescent cells negatively affects non‐senescent cells via reactive oxygen species (ROS). The researchers also show that a paracrine effect of senescent cells can damage DNA.[8][146]
2013 (January) Organization The North American Network in Aging Studies (NANAS) is established with the ultimate purpose to improve the health, care, and quality of life for people aging into old age.[143] United States
2013 Scientific development Laboratory A group of scientists define nine hallmarks of aging that are common between organisms with emphasis on mammals:
2013 Scientific development Silvertown suggests that the ways in which senescence is thought to evolve precludes any common mechanism of decline.[2]
2014 Scientific development Laboratory Researchers report first evidence that pharmacological activation of SIRT1 extends lifespan in mice and improves their health.[123][148][149]
2016 Scientific development Laboratory Scientists at Newcastle University demonstrate for the first time that mitochondria are major triggers of cell aging, after having found that when mitochondria are eliminated from aging cells, the latter become much more similar to younger cells. This discovery advances a step closer to developing therapies to counteract the aging of cells, by targeting mitochondria.[150][151][152] United Kingdom (Newcastle University)
2016 Scientific development Laboratory Researchers find that the replenishment of nicotinamide adenine dinucleotide (NAD+) in the organism of mice through precursor molecules improves the functioning of mitochondria and stem cells, and also leads to an increase in their lifespan.[123][153] One of these NAD+ precursor molecules is nicotinamide mononucleotide NMN.[154][155]
2016 Scientific development Laboratory Researchers demonstrate that a combination of longevity associated drugs can additively extend lifespan in mice.[123][156]
2017 Scientific development Laboratory Researchers discover that a naturally occurring polymorphism in human signaling pathways is in some cases associated with health and longevity. It is also detected that, the same as in mice, this association can depend on the gender (it can be observed for one gender but not for another). This indicates that by correctly influencing these pathways, it is theoretically possible to alter lifespan and healthspan in humans.[123][157]
2017 (December) Scientific development Laboratory Study shows that preventing wrinkles could be as easy as expressing a protein called FKBP1b.[158]
2018 (January) Scientific development Laboratory 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.[159] United States
2018 Policy The World Health Organization includes in the international classification of diseases ICD-11 a special additional code signaling the relationship of a disease with age. As a result, after the final approval of the ICD-11 in May 2019, aging would begin to be officially recognized as a fundamental factor that increases the risk of diseases, the severity of their course and the difficulty of treatment.[160][161][162][163][164]
2018 Scientific development Laboratory Researchers identify naked mole-rats as the first mammal to defy the Gompertz–Makeham law of mortality, and achieve negligible senescence. It would be speculated however that this may be simply a "time-stretching" effect primarily due to their very slow (and cold-blooded and hypoxic) metabolism.[165][166]
Nacktmull.jpg
2019 Scientific development Laboratory Researchers show that many major features of cellular senescence, such as the pro‐inflammatory phenotype, are dependent on the stable cell cycle arrest.[167][8]
2019 Scientific development Laboratory Scientists manage to extend the average lifespan of mice by breeding them using embryonic stem cells with extra-long telomeres. The finding is significant as no genetic modification is conducted.[168][169][170]
2019 (December 9) Scientific development Laboratory Researchers at the Pasteur Institute identify the CSB protein, whose absence or dysfunction causes early aging, among other afflictions, in patients with Cockayne syndrome.[171] France
2020 (July) Scientific development Laboratory Scientists, using public biological data on 1.75 million people with known lifespans overall, identify 10 genomic loci which appear to intrinsically influence healthspan, lifespan, and longevity – of which half have not been reported previously at genome-wide significance and most being associated with cardiovascular disease – and identify haem metabolism as a promising candidate for further research within the field. Their study suggests that high levels of iron in the blood likely reduce, and genes involved in metabolising iron likely increase healthy years of life in humans.[172] United Kingdom
2020 (December) Scientific development Laboratory Researchers at University of California, San Francisco report on an experimental drug called ISRIB, which restores memory function months after traumatic brain injury (TBI) in mice.[173] United States

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References

  1. ↑ 1.0 1.1 1.2 1.3 Andrea Grignolio; Claudio Franceschi. "History of Research into Aging/Senescence". eLS. doi:10.1002/9780470015902.a0023955. 
  2. ↑ 2.00 2.01 2.02 2.03 2.04 2.05 2.06 2.07 2.08 2.09 2.10 2.11 2.12 2.13 Shefferson, Richard P.; Jones, Owen R.; Salguero-Gómez, Roberto (23 February 2017). The Evolution of Senescence in the Tree of Life. Cambridge University Press. ISBN 978-1-107-07850-5. 
  3. ↑ 3.0 3.1 3.2 3.3 A History of Life-Extensionism In The Twentieth Century. Rison Lezion, Israel: Longevity History. 2014. ISBN 1500818577. 
  4. ↑ "Life Expectancy". 
  5. ↑ 5.0 5.1 5.2 5.3 Jin, Kunlin (2010-08-01). "Modern Biological Theories of Aging". Aging and Disease. 1 (2): 72–74. ISSN 2152-5250. 
  6. ↑ Fletcher, James Rupert (December 2020). "Anti-aging technoscience & the biologization of cumulative inequality: Affinities in the biopolitics of successful aging". Journal of Aging Studies. 55: 100899. ISSN 0890-4065. doi:10.1016/j.jaging.2020.100899. 
  7. ↑ Binstock, Robert H. (February 2003). "The War on "Anti-Aging Medicine"". The Gerontologist. 43 (1): 4–14. doi:10.1093/geront/43.1.4. 
  8. ↑ 8.0 8.1 8.2 8.3 8.4 8.5 Ogrodnik, Mikolaj. "Cellular aging beyond cellular senescence: Markers of senescence prior to cell cycle arrest in vitro and in vivo". Aging Cell. 20 (4). doi:10.1111/acel.13338. 
  9. ↑ 9.0 9.1 Handbook of the biology of aging (6th ed.). Amsterdam: Elsevier Academic Press. 2006. ISBN 9780120883875. 
  10. ↑ Fried, Linda P.; Rowe, John W. (2020-10-01). "Health in Aging — Past, Present, and Future". New England Journal of Medicine. 383 (14): 1293–1296. doi:10.1056/NEJMp2016814. 
  11. ↑ Zhavoronkov, Alexander; Bhupinder, Bhullar (4 October 2015). "Classifying aging as a disease in the context of ICD-11". Frontiers in Genetics. 6: 326. PMC 4631811Freely accessible. PMID 26583032. doi:10.3389/fgene.2015.00326. 
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  28. ↑ 28.00 28.01 28.02 28.03 28.04 28.05 28.06 28.07 28.08 28.09 28.10 28.11 28.12 28.13 28.14 28.15 28.16 28.17 28.18 28.19 28.20 28.21 Medvedev, Zhores A. (August 1990). "AN ATTEMPT AT A RATIONAL CLASSIFICATION OF THEORIES OF AGING". Biological Reviews. 65 (3): 375–398. doi:10.1111/j.1469-185x.1990.tb01428.x. 
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  38. ↑ Fossel, Michael. The Telomerase Revolution: The Enzyme That Holds the Key to Human Aging. 
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  86. ↑ Goldsmith, Theodore. The Evolution of Aging: How New Theories Will Change the Future of Medicine. p. 48. 
  87. ↑ Blagosklonny, Mikhail V. (29 December 2010). "Why the disposable soma theory cannot explain why women live longer and why we age". Aging. 2 (12): 884–887. doi:10.18632/aging.100253. 
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  91. ↑ Das, R; Kanungo, MS (June 1980). "In vitro phosphorylation of chromosomal proteins of the brain of rats of various ages & its modulation by epinephrine.". Indian journal of biochemistry & biophysics. 17 (3): 217–21. PMID 7450808. 
  92. ↑ "Alliance for Aging Research". www.idealist.org. Retrieved 8 June 2021. 
  93. ↑ Gavrilov LA, Gavrilova NS (1986). Skulachev WP, ed. Биология продолжительности жизни: Количественные аспекты [Biology of Life Span: Quantitative Aspects] (in русский) (1st ed.). Moscow: Nauka. p. 167. 
  94. ↑ Gavrilov LA, Gavrilova NS (1991). Skulachev VP, ed. Biology of Life Span: A Quantitative Approach (1st ed.). New York: Chur. p. 385. ISBN 978-3718649839. 
  95. ↑ Gavrilov LA, Gavrilova NS (December 2001). "The reliability theory of aging and longevity". Journal of Theoretical Biology. 213 (4): 527–45. PMID 11742523. doi:10.1006/jtbi.2001.2430. 
  96. ↑ A.J.S. Rayl (13 May 2002). "Aging, in Theory: A Personal Pursuit. Do body system redundancies hold the key?" (PDF). The Scientist. 16 (10): 20. 
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