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{{short description|Deterioration of function with age}}
{{about|the aging of whole organisms including animals|aging specifically in humans|
{{Use American English|date=May 2024}}
{{Use dmy dates|date=May 2024}}
{{cs1 config|name-list-style=vanc|display-authors=3}}
▲{{about|the aging of whole organisms including animals|aging specifically in humans|Aging|plants|Plant senescence|cells that stop dividing|Cellular senescence|bacteria|Bacterial senescence}}
'''Senescence''' ({{IPAc-en|s|ɪ|ˈ|n|ɛ|s|ə|n|s}}) or '''biological aging''' is the gradual deterioration of [[Function (biology)|functional]] characteristics in living organisms. Whole [[organism]] senescence involves an increase in [[mortality rate|death rates]]
Environmental [[Gerontogens|factors]] may affect [[aging]] – for example, overexposure to [[ultraviolet radiation]] accelerates [[skin aging]]. Different parts of the body may age at different rates and distinctly, including [[Aging brain|the brain]], [[Cardiovascular disease#Age|the cardiovascular system]], and <!--Skeletal muscle#Atrophy [[Aging musculature]]-->muscle. Similarly, functions may distinctly decline with aging, including [[Aging movement control|movement control]] and [[Memory and aging|memory]]. Two organisms of the same species can also age at different rates, making biological aging and chronological aging distinct concepts.
==Definition and characteristics==
''Organismal senescence'' is the aging of whole organisms. Actuarial senescence can be defined as an increase in mortality
[[Aging]] is characterized by the declining ability to respond to stress, increased [[homeostasis|homeostatic]] imbalance, and increased risk of [[aging-associated diseases]] including [[cancer]] and [[heart disease]]. Aging has been defined as "a progressive deterioration of physiological function, an intrinsic age-related process of loss of viability and increase in vulnerability."<ref>{{Cite web |title=Aging and Gerontology Glossary |url=http://www.senescence.info/glossary.html |access-date=26 February 2011 |archive-date=19 October 2019 |archive-url=https://web.archive.org/web/20191019200702/http://www.senescence.info/glossary.html |url-status=live }}</ref>
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* disabled [[macroautophagy]]
* [[chronic inflammation]]
* [[dysbiosis]]<ref name="10.1016/j.cell.2022.11.001">{{cite journal |last1=López-Otín |first1=Carlos |last2=Blasco |first2=Maria A. |last3=Partridge |first3=Linda |last4=Serrano |first4=Manuel |last5=Kroemer |first5=Guido |title=Hallmarks of aging: An expanding universe |journal=Cell |date=19 January 2023 |volume=186 |issue=2 |pages=243–278 |doi=10.1016/j.cell.2022.11.001 |pmid=36599349 |s2cid=255394876 |language=English
The environment induces damage at various levels, e.g. [[DNA damage theory of aging|damage to DNA]], and damage to tissues and cells by oxygen [[radical (chemistry)|radicals]] (widely known as [[Free-radical theory|free radicals]]), and some of this damage is not repaired and thus accumulates with time.<ref name="pmid1383772">{{cite journal |vauthors=Holmes GE, Bernstein C, Bernstein H |title=Oxidative and other DNA damages as the basis of aging: a review |journal=Mutat. Res. |volume=275 |issue=3–6 |pages=305–15 |date=September 1992 |pmid=1383772 |doi= 10.1016/0921-8734(92)90034-m}}</ref> [[Cloning]] from [[somatic cell]]s rather than germ cells may begin life with a higher initial load of damage. [[Dolly the sheep]] died young from a contagious lung disease, but data on an entire population of cloned individuals would be necessary to measure mortality rates and quantify aging.{{citation needed|date=December 2019}}
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==Variation among species==
{{Further|Longevity#Non-human biological longevity}}
Different speeds with which mortality increases with age correspond to different [[maximum life span]] among [[species]]. For example, a [[mouse]] is elderly at 3 years, a [[human]] is elderly at 80 years,<ref>{{cite journal | vauthors = Austad SN | title = Comparative biology of aging | journal = The Journals of Gerontology. Series A, Biological Sciences and Medical Sciences | volume = 64 | issue = 2 | pages = 199–201 | date = February 2009 | pmid = 19223603 | pmc = 2655036 | doi = 10.1093/gerona/gln060 }}</ref> and [[ginkgo]] trees show little effect of age even at 667 years.<ref name="Wang">{{cite journal | vauthors = Wang L, Cui J, Jin B, Zhao J, Xu H, Lu Z, Li W, Li X, Li L, Liang E, Rao X, Wang S, Fu C, Cao F, Dixon RA, Lin J
Almost all organisms senesce, including [[bacterial senescence|bacteria]] which have asymmetries between "mother" and "daughter" cells upon [[cell division]], with the mother cell experiencing aging, while the daughter is rejuvenated.<ref>{{cite journal | vauthors = Ackermann M, Stearns SC, Jenal U | title = Senescence in a bacterium with asymmetric division | journal = Science | volume = 300 | issue = 5627 | pages = 1920 | date = June 2003 | pmid = 12817142 | doi = 10.1126/science.1083532 | s2cid = 34770745 }}</ref><ref>{{cite journal | vauthors = Stewart EJ, Madden R, Paul G, Taddei F | title = Aging and death in an organism that reproduces by morphologically symmetric division | journal = PLOS Biology | volume = 3 | issue = 2 | pages = e45 | date = February 2005 | pmid = 15685293 | pmc = 546039 | doi = 10.1371/journal.pbio.0030045 | doi-access = free }}</ref> There is [[negligible senescence]] in some groups, such as the genus ''[[Hydra (genus)|Hydra]]''.<ref name="Dańko Kozłowski Schaible 2015 pp. 137–149">{{cite journal | vauthors = Dańko MJ, Kozłowski J, Schaible R | title = Unraveling the non-senescence phenomenon in Hydra | journal = Journal of Theoretical Biology | volume = 382 | pages = 137–49 | date = October 2015 | pmid = 26163368 | doi = 10.1016/j.jtbi.2015.06.043 | bibcode = 2015JThBi.382..137D | doi-access = free }}</ref> [[Planarian]] [[flatworm]]s have "apparently limitless [[telomere]] regenerative capacity fueled by a population of highly proliferative adult [[stem cell]]s."<ref>{{cite journal | vauthors = Tan TC, Rahman R, Jaber-Hijazi F, Felix DA, Chen C, Louis EJ, Aboobaker A | title = Telomere maintenance and telomerase activity are differentially regulated in asexual and sexual worms | journal = Proceedings of the National Academy of Sciences of the United States of America | volume = 109 | issue = 11 | pages = 4209–14 | date = March 2012 | pmid = 22371573 | pmc = 3306686 | doi = 10.1073/pnas.1118885109
Some species exhibit "negative senescence", in which reproduction capability increases or is stable, and mortality falls with age, resulting from the advantages of increased body size during aging.<ref>{{cite journal | vauthors = Vaupel JW, Baudisch A, Dölling M, Roach DA, Gampe J | title = The case for negative senescence | journal = Theoretical Population Biology | volume = 65 | issue = 4 | pages = 339–51 | date = June 2004 | pmid = 15136009 | doi = 10.1016/j.tpb.2003.12.003 | bibcode = 2004TPBio..65..339W }}</ref>
== Theories of aging ==
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More than 300 different theories have been posited to explain the nature (mechanisms) and causes (reasons for natural emergence or factors) of aging.<ref>{{cite journal | vauthors = Viña J, Borrás C, Miquel J | title = Theories of ageing | journal = IUBMB Life | volume = 59 | issue = 4–5 | pages = 249–54 | date = 2007 | pmid = 17505961 | doi = 10.1080/15216540601178067 | doi-access = free }}</ref>{{additional citation needed|date=March 2023}} Good [[Scientific theory|theories]] would both explain past observations and predict the results of future experiments. Some of the theories may complement each other, overlap, contradict, or may not preclude various other theories.{{citation needed|date=March 2023}}
Theories of aging fall into two broad categories, evolutionary theories of aging and mechanistic theories of aging. Evolutionary theories of aging primarily explain why aging happens,<ref>{{Cite journal|last1=Kirkwood|first1=Thomas B. L.|last2=Austad|first2=Steven N.|date=2000|title=Why do we age?|url=http://dx.doi.org/10.1038/35041682|journal=Nature|volume=408|issue=6809|pages=
{{Excerpt|Stem cell theory of aging|Other theories of aging}}
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====Chemical damage====
{{See also|DNA damage theory of aging}}
[[Image:Edward S. Curtis Collection People 086.jpg|thumb|
One of the earliest aging theories was the ''[[Rate-of-living theory|Rate of Living Hypothesis]]'' described by [[Raymond Pearl]] in 1928<ref>{{Cite book| vauthors = Pearl R |title=The Rate of Living, Being an Account of Some Experimental Studies on the Biology of Life Duration|publisher=Alfred A. Knopf|year=1928|location=New York}}{{Page needed|date=September 2010}}</ref> (based on earlier work by [[Max Rubner]]), which states that fast [[basal metabolic rate]] corresponds to short [[maximum life span]].
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With respect to specific types of chemical damage caused by metabolism, it is suggested that damage to long-lived [[biopolymer]]s, such as structural [[protein]]s or [[DNA damage theory of aging|DNA]], caused by ubiquitous chemical agents in the body such as [[oxygen]] and [[sugar]]s, are in part responsible for aging. The damage can include breakage of biopolymer chains, [[cross-link]]ing of biopolymers, or chemical attachment of unnatural substituents ([[hapten]]s) to biopolymers.{{citation needed|date=December 2019}}
Under normal [[wikt:aerobic|aerobic]] conditions, approximately 4% of the [[oxygen]] metabolized by [[mitochondria]] is converted to [[superoxide]] ion, which can subsequently be converted to [[hydrogen peroxide]], [[hydroxyl]] [[radical (chemistry)|radical]] and eventually other reactive species including other [[peroxide]]s and [[singlet oxygen]], which can, in turn, generate [[radical (chemistry)|free radical]]s capable of damaging structural proteins and DNA.<ref name="pmid1383772" /> Certain metal [[ion]]s found in the body, such as [[copper]] and [[iron]], may participate in the process. (In [[Wilson's disease]], a [[genetic disorder|hereditary defect]] that causes the body to retain copper, some of the symptoms resemble accelerated senescence.) These processes termed [[oxidative stress]] are linked to the potential benefits of dietary [[polyphenol]] [[antioxidant]]s, for example in [[coffee]],<ref>{{cite journal | vauthors = Freedman ND, Park Y, Abnet CC, Hollenbeck AR, Sinha R | title = Association of coffee drinking with total and cause-specific mortality | journal = The New England Journal of Medicine | volume = 366 | issue = 20 | pages = 1891–904 | date = May 2012 | pmid = 22591295 | pmc = 3439152 | doi = 10.1056/NEJMoa1112010 }}</ref> and [[green tea|tea]].<ref>{{cite journal | vauthors = Yang Y, Chan SW, Hu M, Walden R, Tomlinson B | title = Effects of some common food constituents on cardiovascular disease | journal = ISRN Cardiology | volume = 2011 | pages = 397136 | year = 2011 | pmid = 22347642 | pmc = 3262529 | doi = 10.5402/2011/397136 | doi-access = free }}</ref> However their typically positive effects on lifespans when consumption is moderate<ref>{{cite journal |last1=Poole |first1=Robin |last2=Kennedy |first2=Oliver J. |last3=Roderick |first3=Paul |last4=Fallowfield |first4=Jonathan A. |last5=Hayes |first5=Peter C. |last6=Parkes |first6=Julie |title=Coffee consumption and health: umbrella review of meta-analyses of multiple health outcomes |journal=BMJ |date=22 November 2017 |volume=359 |pages=j5024 |doi=10.1136/bmj.j5024 |pmid=29167102 |pmc=5696634
[[Sugar]]s such as [[glucose]] and [[fructose]] can react with certain [[amino acid]]s such as [[lysine]] and [[arginine]] and certain DNA bases such as [[guanine]] to produce sugar adducts, in a process called ''[[glycation]]''. These adducts can further rearrange to form reactive species, which can then cross-link the structural proteins or DNA to similar biopolymers or other biomolecules such as non-structural proteins. People with [[diabetes]], who have elevated [[blood sugar]], develop senescence-associated disorders much earlier than the general population, but can delay such disorders by rigorous control of their blood sugar levels. There is evidence that sugar damage is linked to oxidant damage in a process termed ''[[Advanced glycation endproduct|glycoxidation]]''.
[[Reactive oxygen species|Free radicals]] can damage proteins, [[lipid]]s or [[DNA damage theory of aging|DNA]]. [[Glycation]] mainly damages proteins. Damaged proteins and lipids accumulate in [[lysosome]]s as [[lipofuscin]]. Chemical damage to structural proteins can lead to loss of function; for example, damage to [[collagen]] of [[blood vessel]] walls can lead to vessel-wall stiffness and, thus, [[hypertension]], and vessel wall thickening and reactive tissue formation ([[atherosclerosis]]); similar processes in the [[kidney]] can lead to [[kidney failure]]. Damage to [[enzyme]]s reduces cellular functionality. Lipid [[redox|peroxidation]] of the inner [[mitochondrial membrane]] reduces the [[electric potential]] and the ability to generate energy. It is probably no accident that nearly all of the so-called "[[accelerated aging disease]]s" are due to defective [[DNA repair]] enzymes.<ref name="KimuraSuzuki2008">{{cite book|vauthors=Bernstein H, Payne CM, Bernstein C, Garewal H, Dvorak K|url=https://books.google.com/books?id=arjZMwAACAAJ&pg=PA1|title=New Research on DNA Damage|publisher=Nova Science Publishers|year=2008|isbn=978-1604565812|veditors=Kimura H, Suzuki A|pages=1–47|chapter=Cancer and aging as consequences of un-repaired DNA damage.|chapter-url=https://www.novapublishers.com/catalog/product_info.php?products_id=43247|access-date=4 February 2016|archive-date=15 November 2023|archive-url=https://web.archive.org/web/20231115062953/https://books.google.com/books?id=arjZMwAACAAJ&pg=PA1|url-status=live}}</ref><ref name="pmid27164092">{{cite journal | vauthors = Pan MR, Li K, Lin SY, Hung WC | title = Connecting the Dots: From DNA Damage and Repair to Aging | journal = International Journal of Molecular Sciences | volume = 17 | issue = 5 | pages = 685 | date = May 2016 | pmid = 27164092 | pmc = 4881511 | doi = 10.3390/ijms17050685 | doi-access = free }}</ref>
It is believed that the [[impact of alcohol on aging]] can be partly explained by alcohol's activation of the [[HPA axis]], which stimulates [[glucocorticoid]] secretion, long-term exposure to which produces symptoms of aging.<ref>{{cite journal | vauthors = Spencer RL, Hutchison KE | title = Alcohol, aging, and the stress response | journal = Alcohol Research & Health | volume = 23 | issue = 4 | pages = 272–83 | year = 1999 | pmid = 10890824 | pmc = 6760387 | url = http://pubs.niaaa.nih.gov/publications/arh23-4/272-283.pdf | access-date = 8 April 2008 | archive-date = 11 December 2018 | archive-url = https://web.archive.org/web/20181211163358/http://pubs.niaaa.nih.gov/publications/arh23-4/272-283.pdf | url-status = dead }}</ref>
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====DNA damage====
[[DNA damage (naturally occurring)|DNA damage]] was proposed in a 2021 review to be the underlying cause of aging because of the mechanistic link of DNA damage to nearly every aspect of the aging phenotype.<ref name="Schumacher2021">{{Cite journal |last1=Schumacher |first1=Björn |last2=Pothof |first2=Joris |last3=Vijg |first3=Jan |last4=Hoeijmakers |first4=Jan H. J. |date=April 2021 |title=The central role of DNA damage in the ageing process |journal=Nature |volume=592 |issue=7856 |pages=695–703 |doi=10.1038/s41586-021-03307-7
====Mutation accumulation====
{{Main|Mutation accumulation theory}}
[[Natural selection]] can support lethal and harmful [[allele]]s, if their effects are felt after reproduction. The geneticist [[J. B. S. Haldane]] wondered why the dominant mutation that causes [[Huntington's disease]] remained in the population, and why natural selection had not eliminated it. The onset of this neurological disease is (on average) at age 45 and is invariably fatal within 10–20 years. Haldane assumed that, in human prehistory, few survived until age 45. Since few were alive at older ages and their contribution to the next generation was therefore small relative to the large cohorts of younger age groups, the force of selection against such late-acting deleterious mutations was correspondingly small. Therefore, a [[genetic load]] of late-acting deleterious mutations could be substantial at [[mutation–selection balance]]. This concept came to be known as the [[selection shadow]].<ref>{{cite web
[[Peter Medawar]] formalised this observation in his [[Evolution of ageing#Mutation accumulation|mutation accumulation theory]] of aging.<ref>{{Cite journal| vauthors = Medawar PB |year=1946 |title=Old age and natural death |journal=Modern Quarterly |volume=1 |pages=30–56}}</ref><ref>{{
==== Other damage ====
A study concluded that [[retrovirus]]es in the [[human genome]]s can become awakened from dormant states and contribute to aging which can be blocked by [[Neutralizing antibody|neutralizing antibodies]], alleviating "cellular senescence and tissue degeneration and, to some extent, organismal aging".<ref>{{cite journal |last1=Liu |first1=Xiaoqian |last2=Liu |first2=Zunpeng |last3=Wu |first3=Zeming |last4=Ren |first4=Jie |last5=Fan |first5=Yanling |last6=Sun |first6=Liang |last7=Cao |first7=Gang |last8=Niu |first8=Yuyu |last9=Zhang |first9=Baohu |last10=Ji |first10=Qianzhao |last11=Jiang |first11=Xiaoyu |last12=Wang |first12=Cui |last13=Wang |first13=Qiaoran |last14=Ji |first14=Zhejun |last15=Li |first15=Lanzhu |last16=Esteban |first16=Concepcion Rodriguez |last17=Yan |first17=Kaowen |last18=Li |first18=Wei |last19=Cai |first19=Yusheng |last20=Wang |first20=Si |last21=Zheng |first21=Aihua |last22=Zhang |first22=Yong E. |last23=Tan |first23=Shengjun |last24=Cai |first24=Yingao |last25=Song |first25=Moshi |last26=Lu |first26=Falong |last27=Tang |first27=Fuchou |last28=Ji |first28=Weizhi |last29=Zhou |first29=Qi |last30=Belmonte |first30=Juan Carlos Izpisua |last31=Zhang |first31=Weiqi |last32=Qu |first32=Jing |last33=Liu |first33=Guang-Hui |title=Resurrection of endogenous retroviruses during aging reinforces senescence |journal=Cell |date=19 January 2023 |volume=186 |issue=2 |pages=287–304.e26 |doi=10.1016/j.cell.2022.12.017 |pmid=36610399 |s2cid=232060038 |language=English
* Expert explanation of the study: {{cite news |title=Aging and Retroviruses |url=https://www.science.org/content/blog-post/aging-and-retroviruses |access-date=17 February 2023 |work=Science
=== Stem cell theories of aging ===
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{{Main|Biomarkers of aging}}
If different individuals age at different rates, then fecundity, mortality, and functional capacity might be better predicted by [[biomarker]]s than by chronological age.<ref name="Gasmi">{{cite journal | vauthors = Gasmi A, Chirumbolo S, Peana M, Mujawdiya PK, Dadar M, Menzel A, Bjørklund G | title = Biomarkers of Senescence during Aging as Possible Warnings to Use Preventive Measures | journal = Current Medicinal Chemistry | volume = 28 | issue = 8 | pages =
Levels of [[CD4]] and [[CD8]] [[memory T cell]]s and [[naive T cell]]s have been used to give good predictions of the expected lifespan of middle-aged mice.<ref>{{cite journal | vauthors = Miller RA | title = Biomarkers of aging: prediction of longevity by using age-sensitive T-cell subset determinations in a middle-aged, genetically heterogeneous mouse population | journal = The Journals of Gerontology. Series A, Biological Sciences and Medical Sciences | volume = 56 | issue = 4 | pages = B180-6 | date = April 2001 | pmid = 11283189 | pmc = 7537444 | doi = 10.1093/gerona/56.4.b180 | doi-access = free }}</ref>
=== Aging clocks ===
There is interest in an [[epigenetic clock]] as a biomarker of aging, based on its ability to predict human chronological age.<ref
▲There is interest in an [[epigenetic clock]] as a biomarker of aging, based on its ability to predict human chronological age.<ref name="Horvath2013">{{cite journal | vauthors = Horvath S | title = DNA methylation age of human tissues and cell types | journal = Genome Biology | volume = 14 | issue = 10 | pages = R115 | year = 2013 | pmid = 24138928 | pmc = 4015143 | doi = 10.1186/gb-2013-14-10-r115 | doi-access = free }}</ref> Basic blood [[biochemistry]] and cell counts can also be used to accurately predict the chronological age.<ref name="pmid27191382">{{cite journal | vauthors = Putin E, Mamoshina P, Aliper A, Korzinkin M, Moskalev A, Kolosov A, Ostrovskiy A, Cantor C, Vijg J, Zhavoronkov A | display-authors = 6 | title = Deep biomarkers of human aging: Application of deep neural networks to biomarker development | journal = Aging | volume = 8 | issue = 5 | pages = 1021–33 | date = May 2016 | pmid = 27191382 | pmc = 4931851 | doi = 10.18632/aging.100968 }}</ref> It is also possible to predict the human chronological age using transcriptomic aging clocks.<ref>{{cite journal | vauthors = Peters MJ, Joehanes R, Pilling LC, Schurmann C, Conneely KN, Powell J, Reinmaa E, Sutphin GL, Zhernakova A, Schramm K, Wilson YA, Kobes S, Tukiainen T, Ramos YF, Göring HH, Fornage M, Liu Y, Gharib SA, Stranger BE, De Jager PL, Aviv A, Levy D, Murabito JM, Munson PJ, Huan T, Hofman A, Uitterlinden AG, Rivadeneira F, van Rooij J, Stolk L, Broer L, Verbiest MM, Jhamai M, Arp P, Metspalu A, Tserel L, Milani L, Samani NJ, Peterson P, Kasela S, Codd V, Peters A, Ward-Caviness CK, Herder C, Waldenberger M, Roden M, Singmann P, Zeilinger S, Illig T, Homuth G, Grabe HJ, Völzke H, Steil L, Kocher T, Murray A, Melzer D, Yaghootkar H, Bandinelli S, Moses EK, Kent JW, Curran JE, Johnson MP, Williams-Blangero S, Westra HJ, McRae AF, Smith JA, Kardia SL, Hovatta I, Perola M, Ripatti S, Salomaa V, Henders AK, Martin NG, Smith AK, Mehta D, Binder EB, Nylocks KM, Kennedy EM, Klengel T, Ding J, Suchy-Dicey AM, Enquobahrie DA, Brody J, Rotter JI, Chen YD, Houwing-Duistermaat J, Kloppenburg M, Slagboom PE, Helmer Q, den Hollander W, Bean S, Raj T, Bakhshi N, Wang QP, Oyston LJ, Psaty BM, Tracy RP, Montgomery GW, Turner ST, Blangero J, Meulenbelt I, Ressler KJ, Yang J, Franke L, Kettunen J, Visscher PM, Neely GG, Korstanje R, Hanson RL, Prokisch H, Ferrucci L, Esko T, Teumer A, van Meurs JB, Johnson AD | display-authors = 6 | title = The transcriptional landscape of age in human peripheral blood | journal = Nature Communications | volume = 6 | pages = 8570 | date = October 2015 | pmid = 26490707 | pmc = 4639797 | doi = 10.1038/ncomms9570 | bibcode = 2015NatCo...6.8570. }}</ref>
There is research and development of further biomarkers, detection systems and software systems to measure biological age of different tissues or systems or overall. For example, a [[deep learning]] (DL) software using anatomic [[magnetic resonance image]]s estimated [[brain aging|brain age]] with relatively high accuracy, including detecting early signs of Alzheimer's disease and varying [[neuroanatomical]] patterns of neurological aging,<ref>{{cite journal |last1=Yin |first1=Chenzhong |last2=Imms |first2=Phoebe |last3=Cheng |first3=Mingxi |display-authors=et al. |title=Anatomically interpretable deep learning of brain age captures domain-specific cognitive impairment |journal=Proceedings of the National Academy of Sciences |date=10 January 2023 |volume=120 |issue=2 |pages=e2214634120 |doi=10.1073/pnas.2214634120 |pmid=36595679 |pmc=9926270 |bibcode=2023PNAS..12014634Y
* University press release: {{cite news |title=How old is your brain, really? AI-powered analysis accurately reflects risk of cognitive decline and Alzheimer's disease |url=https://medicalxpress.com/news/2023-01-brain-ai-powered-analysis-accurately-cognitive.html |access-date=17 February 2023 |work=University of Southern California via medicalxpress.com
* News article about the study: {{cite news |title=KI kann wahres Alter des Hirns bestimmen |url=https://www.deutschlandfunknova.de/nachrichten/alterungsprozess-ki-kann-wahres-alter-des-hirns-bestimmen |access-date=17 February 2023 |work=[[Deutschlandfunk Nova]] |language=de |archive-date=17 February 2023 |archive-url=https://web.archive.org/web/20230217232037/https://www.deutschlandfunknova.de/nachrichten/alterungsprozess-ki-kann-wahres-alter-des-hirns-bestimmen |url-status=live }}</ref> and a DL tool was reported as to calculate a person's [[Inflammaging|inflammatory age]] based on patterns of systemic age-related inflammation.<ref>{{cite journal |last1=Sayed |first1=Nazish |last2=Huang |first2=Yingxiang |last3=Nguyen |first3=Khiem |last4=Krejciova-Rajaniemi |first4=Zuzana |last5=Grawe |first5=Anissa P. |last6=Gao |first6=Tianxiang |last7=Tibshirani |first7=Robert |last8=Hastie |first8=Trevor |last9=Alpert |first9=Ayelet |last10=Cui |first10=Lu |last11=Kuznetsova |first11=Tatiana |last12=Rosenberg-Hasson |first12=Yael |last13=Ostan |first13=Rita |last14=Monti |first14=Daniela |last15=Lehallier |first15=Benoit |last16=Shen-Orr |first16=Shai S. |last17=Maecker |first17=Holden T. |last18=Dekker |first18=Cornelia L. |last19=Wyss-Coray |first19=Tony |last20=Franceschi |first20=Claudio |last21=Jojic |first21=Vladimir |last22=Haddad |first22=François |last23=Montoya |first23=José G. |last24=Wu |first24=Joseph C. |last25=Davis |first25=Mark M. |last26=Furman |first26=David |title=An inflammatory aging clock (iAge) based on deep learning tracks multimorbidity, immunosenescence, frailty and cardiovascular aging |journal=Nature Aging |date=July 2021 |volume=1 |issue=7 |pages=598–615 |doi=10.1038/s43587-021-00082-y |pmid=34888528 |pmc=8654267
* News article about the study: {{cite news |title=Tool that calculates immune system age could predict frailty and disease |url=https://newatlas.com/science/stanford-immune-system-age-biomarker-blood-test/ |access-date=26 July 2021 |work=New Atlas |date=13 July 2021 |archive-date=26 July 2021 |archive-url=https://web.archive.org/web/20210726110032/https://newatlas.com/science/stanford-immune-system-age-biomarker-blood-test/ |url-status=live }}</ref>
Aging clocks have been used to evaluate impacts of interventions on humans, including [[combination therapy|combination therapies]].<ref>{{cite journal |title=Potential reversal of epigenetic age using a diet and lifestyle intervention: a pilot randomized clinical trial |journal=Aging |year=2021 |pmid=33844651 |url=https://www.aging-us.com/article/202913/text |access-date=28 June 2021 |last1=Fitzgerald |first1=K. N. |last2=Hodges |first2=R. |last3=Hanes |first3=D. |last4=Stack |first4=E. |last5=Cheishvili |first5=D. |last6=Szyf |first6=M. |last7=Henkel |first7=J. |last8=Twedt |first8=M. W. |last9=Giannopoulou |first9=D. |last10=Herdell |first10=J. |last11=Logan |first11=S. |last12=Bradley |first12=R. |volume=13 |issue=7 |pages=
==Genetic determinants of aging==
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This report suggests that [[DNA damage]], not [[oxidative stress]], is the cause of this form of accelerated aging.
A study indicates that aging may shift activity toward short genes or shorter transcript length and that this can be countered by interventions.<ref>{{cite journal |last1=Stoeger |first1=Thomas |last2=Grant |first2=Rogan A. |last3=McQuattie-Pimentel |first3=Alexandra C. |last4=Anekalla |first4=Kishore R. |last5=Liu |first5=Sophia S. |last6=Tejedor-Navarro |first6=Heliodoro |last7=Singer |first7=Benjamin D. |last8=Abdala-Valencia |first8=Hiam |last9=Schwake |first9=Michael |last10=Tetreault |first10=Marie-Pier |last11=Perlman |first11=Harris |last12=Balch |first12=William E. |last13=Chandel |first13=Navdeep S. |last14=Ridge |first14=Karen M. |last15=Sznajder |first15=Jacob I. |last16=Morimoto |first16=Richard I. |last17=Misharin |first17=Alexander V. |last18=Budinger |first18=G. R. Scott |last19=Nunes Amaral |first19=Luis A. |title=Aging is associated with a systemic length-associated transcriptome imbalance |journal=Nature Aging |date=December 2022 |volume=2 |issue=12 |pages=1191–1206 |doi=10.1038/s43587-022-00317-6 |pmid=37118543 |pmc=10154227
* University press release: {{cite news |title=Aging is driven by unbalanced genes, finds AI analysis of multiple species |url=https://phys.org/news/2022-12-aging-driven-unbalanced-genes-ai.html |access-date=18 January 2023 |work=[[Northwestern University]] |via=phys.org |date=December 9, 2022
* News article about the study: {{cite news |last1=Kwon |first1=Diana |title=Aging Is Linked to More Activity in Short Genes Than in Long Genes |url=https://www.scientificamerican.com/article/aging-is-linked-to-more-activity-in-short-genes-than-in-long-genes/ |url-access=subscription |date=January 6, 2023 |access-date=18 January 2023 |work=Scientific American
== Healthspans and aging in society ==
[[File:Global aging demographics.webp|thumb|Past and projected age of the human world population through time as of 2021<ref name="10.1038/s41536-021-00169-5">{{cite journal |last1=Garmany |first1=Armin |last2=Yamada |first2=Satsuki |last3=Terzic |first3=Andre |title=Longevity leap: mind the healthspan gap |journal=npj Regenerative Medicine |date=23 September 2021 |volume=6 |issue=1 |page=57 |doi=10.1038/s41536-021-00169-5 |pmid=34556664 |pmc=8460831
* Non-profit hospital press release: {{cite news |first1=Susan |last1=Buckles |title=A regenerative reset for aging » Center for Regenerative Biotherapeutics |url=https://regenerativemedicineblog.mayoclinic.org/2021/10/07/a-regenerative-reset-for-aging |date=October 7, 2021 |access-date=1 March 2023 |work=[[Mayo Clinic]] |archive-date=1 March 2023 |archive-url=https://web.archive.org/web/20230301172642/https://regenerativemedicineblog.mayoclinic.org/2021/10/07/a-regenerative-reset-for-aging/ |url-status=live }}</ref>]]
[[File:Healthspan-lifespan gap.webp|thumb|Healthspan-lifespan gap (LHG)<ref name="10.1038/s41536-021-00169-5"/>]]
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{{Excerpt|Global health|Multimorbidity, age-related diseases and aging|paragraphs=2|only=paragraphs}} <!--The last stages of life are often "racked with chronic, age-related diseases that diminish quality of life" which also-->Biological aging or the LHG comes with a great cost burden to society, including potentially rising health care costs (also depending on types and [[medical costs|costs of treatments]]).<ref name="10.1038/s41536-021-00169-5"/><ref name="10.1016/j.tcb.2016.05.002"/> This, along with global [[quality of life]] or [[wellbeing]], highlight the importance of extending healthspans.<ref name="10.1038/s41536-021-00169-5"/>
Many measures that may extend lifespans may simultaneously also extend healthspans, albeit that is not necessarily the case, indicating that "lifespan can no longer be the sole parameter of interest" in related research.<ref>{{cite journal |last1=Bansal |first1=Ankita |last2=Zhu |first2=Lihua J. |last3=Yen |first3=Kelvin |last4=Tissenbaum |first4=Heidi A. |title=Uncoupling lifespan and healthspan in Caenorhabditis elegans longevity mutants |journal=Proceedings of the National Academy of Sciences |date=20 January 2015 |volume=112 |issue=3 |pages=E277-86 |doi=10.1073/pnas.1412192112 |pmid=25561524 |pmc=4311797 |bibcode=2015PNAS..112E.277B
== Interventions ==
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{{Wiktionary}}
{{Commons category}}
{{Senescence}}
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