{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,11,5]],"date-time":"2026-11-05T00:18:36Z","timestamp":1793837916899,"version":"4.6.1"},"reference-count":536,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2023,4,17]],"date-time":"2023-04-17T00:00:00Z","timestamp":1681689600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"funder":[{"DOI":"10.13039\/100020068","name":"Benter Foundation","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100020068","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Biological Reviews"],"published-print":{"date-parts":[[2023,8]]},"abstract":"<jats:title>ABSTRACT<\/jats:title><jats:p>The characteristic maximum lifespan varies enormously across animal species from a few hours to hundreds of years. This argues that maximum lifespan, and the ageing process that itself dictates lifespan, are to a large extent genetically determined. Although controversial, this is supported by firm evidence that semelparous species display evolutionarily programmed ageing in response to reproductive and environmental cues. Parabiosis experiments reveal that ageing is orchestrated systemically through the circulation, accompanied by programmed changes in hormone levels across a lifetime. This implies that, like the circadian and circannual clocks, there is a master \u2018clock of age\u2019 (circavital clock) located in the limbic brain of mammals that modulates systemic changes in growth factor and hormone secretion over the lifespan, as well as systemic alterations in gene expression as revealed by genomic methylation analysis. Studies on accelerated ageing in mice, as well as human longevity genes, converge on evolutionarily conserved fibroblast growth factors (FGFs) and their receptors, including KLOTHO, as well as insulin\u2010like growth factors (IGFs) and steroid hormones, as key players mediating the systemic effects of ageing. Age\u2010related changes in these and multiple other factors are inferred to cause a progressive decline in tissue maintenance through failure of stem cell replenishment. This most severely affects the immune system, which requires constant renewal from bone marrow stem cells. Age\u2010related immune decline increases risk of infection whereas lifespan can be extended in germfree animals. This and other evidence suggests that infection is the major cause of death in higher organisms. Immune decline is also associated with age\u2010related diseases. Taking the example of Alzheimer's disease (AD), we assess the evidence that AD is caused by immunosenescence and infection. The signature protein of AD brain, A\u03b2, is now known to be an antimicrobial peptide, and A\u03b2 deposits in AD brain may be a response to infection rather than a cause of disease. Because some cognitively normal elderly individuals show extensive neuropathology, we argue that the location of the pathology is crucial \u2013 specifically, lesions to limbic brain are likely to accentuate immunosenescence, and could thus underlie a vicious cycle of accelerated immune decline and microbial proliferation that culminates in AD. This general model may extend to other age\u2010related diseases, and we propose a general paradigm of organismal senescence in which declining stem cell proliferation leads to programmed immunosenescence and mortality.<\/jats:p>","DOI":"10.1111\/brv.12959","type":"journal-article","created":{"date-parts":[[2023,4,18]],"date-time":"2023-04-18T00:40:06Z","timestamp":1681778406000},"page":"1424-1458","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":34,"title":["Programmed ageing: decline of stem cell renewal, immunosenescence, and Alzheimer's disease"],"prefix":"10.1111","volume":"98","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-9698-9834","authenticated-orcid":false,"given":"Richard","family":"Lathe","sequence":"first","affiliation":[{"name":"Division of Infection Medicine, Chancellor's Building University of Edinburgh Medical School Little France Edinburgh EH16 4SB UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David","family":"St. Clair","sequence":"additional","affiliation":[{"name":"Institute of Medical Sciences, School of Medicine University of Aberdeen Aberdeen AB25 2ZD UK"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2023,4,17]]},"reference":[{"key":"e_1_2_8_3_1","volume-title":"Psychoneuroimmunology","author":"Ader R.","year":"1991"},{"key":"e_1_2_8_4_1","doi-asserted-by":"publisher","DOI":"10.1093\/brain\/aww083"},{"key":"e_1_2_8_5_1","doi-asserted-by":"publisher","DOI":"10.1017\/CBO9781139003353.021"},{"key":"e_1_2_8_6_1","doi-asserted-by":"publisher","DOI":"10.1002\/cne.901370404"},{"key":"e_1_2_8_7_1","unstructured":"Alzforum(2014).Immunotherapy II: active approaches down new passive crops up.Alzforum Electronic file available athttps:\/\/www.alzforum.org\/news\/conference-coverage\/immunotherapy-ii-active-approaches-down-new-passive-cropsPublished online 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