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dc.contributor.authorArslan-Ergul, A.en_US
dc.contributor.authorErbaba, B.en_US
dc.contributor.authorKaroglu, E. T.en_US
dc.contributor.authorHalim, D. O.en_US
dc.contributor.authorAdams, M. M.en_US
dc.date.accessioned2018-04-12T10:53:47Z
dc.date.available2018-04-12T10:53:47Z
dc.date.issued2016-10en_US
dc.identifier.issn0306-4522
dc.identifier.urihttp://hdl.handle.net/11693/36800
dc.description.abstractBrain aging is marked by a decline in cognitive abilities and associated with neurodegenerative disorders. Recent studies have shown, neurogenesis continues into adulthood but is known to be decreasing during advancing age and these changes may contribute to cognitive alterations. Advances, which aim to promote better aging are of paramount importance. Dietary restriction (DR) is the only non-genetic intervention that reliably extends life- and health-span. Mechanisms of how and why DR and age affect neurogenesis are not well-understood, and have not been utilized much in the zebrafish, which has become a popular model to study brain aging and neurodegenerative disease due to widely available genetic tools. In this study we used young (8–8.5 months) and old (26–32.5 months) zebrafish as the model to investigate the effects of a short-term DR on actively proliferating cells. We successfully applied a 10-week DR to young and old fish, which resulted in a significant loss of body weight in both groups with no effect on normal age-related changes in body growth. We found that age decreased cell proliferation and increased senescence associated β-galactosidase, as well as shortened telomere lengths. In contrast, DR shortened telomere lengths only in young animals. Neither age nor DR changed the differentiation patterns of glial cells. Our results suggest that the potential effects of DR could be mediated by telomere regulation and whether these are beneficial or negative remains to be determined.en_US
dc.language.isoEnglishen_US
dc.source.titleNeuroscienceen_US
dc.relation.isversionofhttps://doi.org/10.1016/j.neuroscience.2016.07.033en_US
dc.subjectAgingen_US
dc.subjectBrainen_US
dc.subjectCell proliferationen_US
dc.subjectDietary restrictionen_US
dc.subjectTelomereen_US
dc.subjectZebrafishen_US
dc.subjectBeta galactosidaseen_US
dc.subjectBeta galactosidaseen_US
dc.subjectAdulten_US
dc.subjectAgeen_US
dc.subjectAnimal cellen_US
dc.subjectAnimal experimenten_US
dc.subjectArticleen_US
dc.subjectBody growthen_US
dc.subjectBrain regionen_US
dc.subjectBrain sliceen_US
dc.subjectCell differentiationen_US
dc.subjectCell proliferationen_US
dc.subjectControlled studyen_US
dc.subjectDiet restrictionen_US
dc.subjectFish modelen_US
dc.subjectGlia cellen_US
dc.subjectNonhumanen_US
dc.subjectPriority journalen_US
dc.subjectSenescenceen_US
dc.subjectStressen_US
dc.subjectTelomere homeostasisen_US
dc.subjectWeight reductionen_US
dc.subjectZebra fishen_US
dc.subjectAgingen_US
dc.subjectAnimalen_US
dc.subjectBody weighten_US
dc.subjectBrainen_US
dc.subjectCaloric restrictionen_US
dc.subjectCell agingen_US
dc.subjectCohort analysisen_US
dc.subjectMetabolismen_US
dc.subjectPhysiologyen_US
dc.subjectRandomizationen_US
dc.subjectTelomereen_US
dc.subjectTime factoren_US
dc.titleShort-term dietary restriction in old zebrafish changes cell senescence mechanismsen_US
dc.typeArticleen_US
dc.departmentDepartment of Psychology
dc.departmentUNAM - Institute of Materials Science and Nanotechnology
dc.departmentInterdisciplinary Neuroscience Program
dc.departmentDepartment of Molecular Biology and Genetics
dc.citation.spage64en_US
dc.citation.epage75en_US
dc.citation.volumeNumber334en_US
dc.identifier.doi10.1016/j.neuroscience.2016.07.033en_US
dc.publisherElsevieren_US


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