Difference between revisions of "Timeline of senescence research"

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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

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]

Google Ngram Viewer

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

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]

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]
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
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 + b^x. 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 b^x 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
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
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
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
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]
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)
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]
1956	Scientific development		Puck and Markus solve the problem of identifying all forms of cell death, by developing an assay based on the ability of a single cell to grow into a colony. This "clonogenic assay" would form the basis of in vitro cellular response studies in tumors and also some normal tissues.^[56]
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]^[57] 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]^[58]
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.^[59]	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,^[60] 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.^[61]	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.^[62]^[63]^[64]	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.^[65]^[66]
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.^[67]		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.^[68] PCD consists in any active cellular process that culminates in cell death.^[69]	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.^[70]^[71]
1965–1969	Scientific development	Laboratory	The strong effect of age on DNA methylation levels is discovered,^[72] thus rendering it an accurate biological clock in humans and chimpanzees.^[73]
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.^[74] This theory becomes stronger through further experimental support during the following decades.^[75]^[76]
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.^[77] It is well documented that the effectiveness of the immune system peaks at puberty and gradually declines thereafter with advance in age.^[78]	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.^[79]	United States
1972	Scientific development		Kerr, Wyllie, and Currie first coin the term “apoptosis” to differentiate naturally occurring developmental cell death from the necrosis that results from acute tissue injury. They also note that apoptosis is responsible for maintaining tissue homeostasis by mediating the equilibrium between cell proliferation and cell death in a particular tissue.^[56]
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.^[80]^[81]	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.^[82]^[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.^[83]^[84] 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.^[85] Further experiments establish the role of telomere shortening in cellular aging and telomerase reactivation in cell immortalization.^[86]	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.^[87] 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.^[88] This theory would be further developed in substantial detail (Flatt et al. 2013; Kirkwood 1981, 1985, 2002, 2005; Kirkwood & Holliday 1979; Kirkwood & Rose 1991).^[2]
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.^[67]
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.^[89]
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.^[90]^[91]	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.^[67]
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]^[92]
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]
1981			Lee Eberhardt stresses the need of including senescence when assessing population dynamics, as senescence is expected to have strong implications for conservation and management of mammalian populations. In particular, the occurrence of actuarial and reproductive senescence is expected to lead to a decrease in individual fitness and population growth rates.^[2]
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.^[93]	United States
1986	Scientific development	Theory	The Reliability theory of aging and longevity is proposed by Leonid Gavrilov and Natalia Gavrilova.^[94]^[95]^[96]^[97]
1987	Scientific development	Laboratory	B.M. Stanulis-Praeger determines cell death to be a primary consequence of senescence.^[98]	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.^[67]
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.^[99]
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]^[100]
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.^[101]	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.^[102]
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.^[103]^[104]
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.^[105]	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.^[106]^[107]	United States
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.^[108]
1994	Scientific development		Frisch and Francis report that loss of matrix attachment results in apoptosis. Since then, studies aimed at understanding the molecular mechanisms underlying the phenomenon coupled with advances in the field of apoptosis overall would help to elucidate several of the key players and to create hypotheses for how they are regulated.^[56]
1995	Scientific development	Laboratory	Detection of senescent cells using a cytochemical assay is first described.^[109] 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.^[110]
1995	Scientific development	Laboratory	The existence of senescence-associated beta-galactosidase is proposed by Dimri et al.^[111] 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.^[112]^[113]^[114]
1995	Scientific development	Theory	The remodeling theory of aging is introduced.^[99] It postulates that immunosenescence or 'immuno-remodelling' is a dynamic process involving both loss and gains of immune function.^[115]
1995			Slade suggests that actuarial senescence may be negligible in small mammals.^[2]
1995	Scientific development	Laboratory	Research by by E. Wang shows that cellular senescence is associated with a reduced sensitivity to cell death.^[8]^[116]
1998	Scientific development	Laboratory	Scientists manage to extend, in a laboratory environment, the life of normal human cells beyond the Hayflick limit using telomerase.^[117]^[118]
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]
1998			Caleb Finch, and later other gerontologists and some demographers, argue that there is evidence of negligible senescence in natural populations of a number of species, from rockfish to tortoises.^[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.^[119]^[120]	United States
1999	Literature		Aubrey de Grey publishes The Mitochondrial Free Radical Theory of Aging, which introduces the term "engineered negligible senescence".^[121]
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.^[122]^[123]	United States
2003	Scientific development	Laboratory	Scientists report first evidence that aging of nematodes is regulated via mechanistic target ofrapamycin (mTOR) signaling.^[124]^[125]^[126]
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.^[127] Translated to human standards, such longevity is equivalent to about 180 years.^[128]
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.^[129] 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.^[130]
2004			Reznick et al. suggest the need to develop ecologically oriented "derived" theories of ageing that include density- and condition-dependent interactions with senescent mortality. They state that density dependence affects aging because it interacts with the age profile of mortality and can lead to changes in resource availability. Also, like density dependence, they state that condition dependence can interact with extrinsic mortality and the rate of aging.^[2]
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.^[131]	Germany
2006	Literature (journal)	Clinical study	Peer-reviewed open access medical journal Clinical Interventions in Aging is founded, covering research in gerontology.^[132]
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.^[133] Yamanaka is the first to produce induced stem cells (iSC) from somatic cells by the simultaneous action of several factors.^[134]^[135]^[136]
2007	Scientific development	Laboratory	Researchers manage to extend mouse lifespan via deletion of insulin receptor in the brain.^[124]^[137]
2007	Scientific development		Study by Passos, Saretzki, and Ahmed et al. indicates that mitochondrial-derived reactive oxygen species can generate DNA damage, including single-stranded breaks in telomere regions, contributing to accelerated telomere shortening and premature senescence.^[138]^[139]	United Kingdom (University of Newcastle)
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.^[124]^[140]
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.^[141]	United States
2008	Scientific development		Coppe, Patil, Rodier et al. determine that senescent cells are known to secrete a number of proinflammatory molecules, a phenotype commonly known as the senescence-associated secretory phenotype (SASP).^[138]^[142]
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.^[143]	Germany
2008	Scientific development		Ricklefs, comparing age-related mortality patterns in birds in captivity and wild populations finds that the rate of senescence is similar to that in wild populations despite the absence of exogenous forces of mortality (i.e. predation, disease) in captivity.^[2]
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."^[144] 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]
2009	Scientific development	Laboratory	Researchers report association of genetic variants in insulin/IGF1 signaling with human longevity.^[124]^[145]
2010	Scientific development	Laboratory	Harvard scientists reverse aging process in mice through reactivation of telomerase.^[146]	United States
2010	Scientific development		Study by Passos, Nelson, Wang, et al. reports that reactive oxygen species produced by senescent cells are shown to lock senescent cells in a state of irreversible arrest by contributing to a persistent activation of a DNA damage response.^[138]^[147]
2010	Organization (research network)		The European Network in Aging Studies is established.^[148]^[149]	Europe
2011	Scientific development		Study by Baker, Wijshake, and Tchkonia et al.^[150] (confirmed later by Baker, Childs, and Durik et al. in 2016^[151]) reports that senescent cells accumulate with age and at sites of pathology, where they are shown to drive tissue deterioration.^[138]
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.^[152]	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]^[153]	United Kingdom (Newcastle University)
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.^[148]	United States
2013	Scientific development	Laboratory	A group of scientists define nine hallmarks of aging that are common between organisms with emphasis on mammals: genomic instability, telomere attrition, epigenetic alterations, loss of proteostasis, deregulated nutrient sensing, mitochondrial dysfunction, cellular senescence, stem cell exhaustion, altered intercellular communication.^[154]
2013	Scientific development		Silvertown suggests that the ways in which senescence is thought to evolve precludes any common mechanism of decline.^[2]
2013	Scientific development		Nussey et al. conduct literature survey, and find clear evidence of actuarial senescence (senescence in survival) in large mammalian species (i.e. ungulates, marine mammals and primates).^[2]
2014	Scientific development	Laboratory	Researchers report first evidence that pharmacological activation of SIRT1 extends lifespan in mice and improves their health.^[124]^[155]^[156]
2014	Scientific development		Study by Correia-Melo, Hewitt, and Passos indicates that senescence is a multilayered process which involves dramatic time-dependent changes in gene expression, epigenetic and metabolic profile.^[138]
2015	Scientific development		Study by Madeo, Zimmermann, Maiuri and Kroemer determines that autophagy plays an important role during senescence through the elimination of old or unneeded materials.^[157]
2015	Scientific development		Study by Xu, Palmer, and Ding et al.^[158] (later confirmed by Baker, Childs, and Durik et al.^[159]) indicates that the accumulation of senescent cells in multiple tissues contributes causally to age-related tissue dysfunction.^[138]
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.^[160]^[161]^[162]	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.^[124]^[163] One of these NAD⁺ precursor molecules is nicotinamide mononucleotide NMN.^[164]^[165]
2016	Scientific development	Laboratory	Researchers demonstrate that a combination of longevity associated drugs can additively extend lifespan in mice.^[124]^[166]
2016	Scientific development		Study by Childs, Baker, and Wijshake et al. concludes that senescent intimal foam cells are deleterious at all stages of atherosclerosis.^[138]^[167]
2016	Scientific development		Correia-Melo, Marques, Anderson et al. determine that mitochondria are the powerhouses of cells and are essential for the development of cellular senescence.^[138]^[168]
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.^[124]^[169]
2017	Scientific development		Study by Jeon, Kim, and Laberge et al. reports that senescent cells accumulate in many vertebrate tissues with age and contribute to age-related pathologies, presumably through their secretion of factors contributing to the senescence-associated secretory phenotype,^[170] the latter which defines the ability of senescent cells to express and secrete a variety of extracellular modulators that includes cytokines, chemokines, proteases, growth factors and bioactive lipids.^[171]
2017 (December)	Scientific development	Laboratory	Study shows that preventing wrinkles could be as easy as expressing a protein called FKBP1b.^[172]
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.^[173]	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.^[174]^[175]^[176]^[177]^[178]
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.^[179]^[180]
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.^[181]^[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.^[182]^[183]^[184]
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.^[185]	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.^[186]	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.^[187]	United States

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References

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Category:Senescence Category:Medicine timelines

[history-of-research-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.

[Shefferson-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 ^2.14 ^2.15 ^2.16 ^2.17 ^2.18 ^2.19 ^2.20 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.

[ilia-stambler-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".

[kunlin-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.

[Anti-agi-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.

[Ogrodnik-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.

[Handbook_of_the-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 4631811. PMID 26583032. doi:10.3389/fgene.2015.00326.

[12] Stambler, Ilia (1 October 2017). "Recognizing Degenerative Aging as a Treatable Medical Condition: Methodology and Policy". Aging and Disease. 8 (5): 583–589. PMC 5614323. PMID 28966803. doi:10.14336/AD.2017.0130.

[13] "Opening the door to treating ageing as a disease". The Lancet Diabetes & Endocrinology. 6 (8): 587. 1 August 2018. doi:10.1016/S2213-8587(18)30214-6.

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@@ Line 210: / Line 210: @@
 | 1966 || Scientific development || [[w:Category:Theories of biological aging|Theory]] || Sacher introduces the Wear and tear theory of aging, which is considered an important theory at the whole animal level.<ref name="Dazhong"/> ||
 |-
-| 1966 || Scientific development || || William Hamilton lays out the mathematics drawing on the ideas of [[wikipedia:George C. Williams (biologist)|George C. Williams]] and {{w|Peter Medawar}}, leading to the outcome that "senescence is an inevitable outcome of evolution".<ref name="Shefferson"/>
+| 1966 || Scientific development || || William Hamilton lays out the mathematics drawing on the ideas of [[wikipedia:George C. Williams (biologist)|George C. Williams]] and {{w|Peter Medawar}}, leading to the outcome that "senescence is an inevitable outcome of evolution".<ref name="Shefferson"/> ||
 |-
 | 1967 || Scientific development || [[w:Category:Theories of biological aging|Theory]] || C. Alexander sets the grounds of the {{w|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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