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dc.contributor.authorBonkowski, Michael S.
dc.contributor.authorPointer, Kelli
dc.contributor.authorPletcher, Scott D.
dc.contributor.authorLibert, Sergiy V.
dc.contributor.authorGuarente, Leonard Pershing
dc.date.accessioned2014-02-03T13:29:12Z
dc.date.available2014-02-03T13:29:12Z
dc.date.issued2012-07
dc.date.submitted2012-05
dc.identifier.issn14749718
dc.identifier.issn1474-9728
dc.identifier.urihttp://hdl.handle.net/1721.1/84637
dc.description.abstractThe variation of individual life spans, even in highly inbred cohorts of animals and under strictly controlled environmental conditions, is substantial and not well understood. This variation in part could be due to epigenetic variation, which later affects the animal’s physiology and ultimately longevity. Identification of the physiological properties that impact health and life span is crucial for longevity research and the development of anti-aging therapies. Here, we measured individual circadian and metabolic characteristics in a cohort of inbred F1 hybrid mice and correlated these parameters to their life spans. We found that mice with innate circadian periods close to 24 h (revealed during 30 days of housing in total darkness) enjoyed nearly 20% longer life spans than their littermates, which had shorter or longer innate circadian periods. These findings show that maintenance of a 24-h intrinsic circadian period is a positive predictor of longevity. Our data suggest that circadian period may be used to predict individual longevity and that processes that control innate circadian period affect aging.en_US
dc.description.sponsorshipLeukemia & Lymphoma Society of America (Fellowship 5089-09)en_US
dc.description.sponsorshipEllison Medical Foundation (American Federation for Aging Research Fellowship)en_US
dc.description.sponsorshipNational Institutes of Health (U.S.)en_US
dc.description.sponsorshipPaul F. Glenn Foundationen_US
dc.language.isoen_US
dc.publisherWiley Blackwellen_US
dc.relation.isversionofhttp://dx.doi.org/10.1111/j.1474-9726.2012.00846.xen_US
dc.rightsCreative Commons Attribution-Noncommercial-Share Alike 3.0en_US
dc.rights.urihttp://creativecommons.org/licenses/by-nc-sa/3.0/en_US
dc.sourcePMCen_US
dc.titleDeviation of innate circadian period from 24 hours reduces longevity in miceen_US
dc.title.alternativeDeviation of innate circadian period from 24 h reduces longevity in miceen_US
dc.typeArticleen_US
dc.identifier.citationLibert, Sergiy, Michael S. Bonkowski, Kelli Pointer, Scott D. Pletcher, and Leonard Guarente. “Deviation of innate circadian period from 24 h reduces longevity in mice.” Aging Cell 11, no. 5 (October 12, 2012): 794-800.en_US
dc.contributor.departmentMassachusetts Institute of Technology. Department of Biologyen_US
dc.contributor.departmentPaul F. Glenn Center for Biology of Aging Research (Massachusetts Institute of Technology)en_US
dc.contributor.mitauthorLibert, Sergiy V.en_US
dc.contributor.mitauthorBonkowski, Michael S.en_US
dc.contributor.mitauthorPointer, Kellien_US
dc.contributor.mitauthorGuarente, Leonard Pershingen_US
dc.relation.journalAging Cellen_US
dc.eprint.versionAuthor's final manuscripten_US
dc.type.urihttp://purl.org/eprint/type/JournalArticleen_US
eprint.statushttp://purl.org/eprint/status/PeerRevieweden_US
dspace.orderedauthorsLibert, Sergiy; Bonkowski, Michael S.; Pointer, Kelli; Pletcher, Scott D.; Guarente, Leonarden_US
dc.identifier.orcidhttps://orcid.org/0000-0003-4064-2510
mit.licenseOPEN_ACCESS_POLICYen_US
mit.metadata.statusComplete


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