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Tytuł pozycji:

Short-term dietary restriction in old zebrafish changes cell senescence mechanisms.

Tytuł:
Short-term dietary restriction in old zebrafish changes cell senescence mechanisms.
Autorzy:
Arslan-Ergul A; Bilkent University, Interdisciplinary Neuroscience Program, Ankara, Turkey; Bilkent University, Molecular Biology and Genetics Department Zebrafish Facility, Ankara, Turkey; Bilkent University, UNAM-Institute of Materials Science and Nanotechnology, Ankara, Turkey. Electronic address: .
Erbaba B; Bilkent University, Interdisciplinary Neuroscience Program, Ankara, Turkey; Bilkent University, Molecular Biology and Genetics Department Zebrafish Facility, Ankara, Turkey; Bilkent University, UNAM-Institute of Materials Science and Nanotechnology, Ankara, Turkey. Electronic address: .
Karoglu ET; Bilkent University, Interdisciplinary Neuroscience Program, Ankara, Turkey; Bilkent University, Molecular Biology and Genetics Department Zebrafish Facility, Ankara, Turkey; Bilkent University, UNAM-Institute of Materials Science and Nanotechnology, Ankara, Turkey. Electronic address: .
Halim DO; Bilkent University, Department of Molecular Biology and Genetics, Ankara, Turkey. Electronic address: .
Adams MM; Bilkent University, Interdisciplinary Neuroscience Program, Ankara, Turkey; Bilkent University, Molecular Biology and Genetics Department Zebrafish Facility, Ankara, Turkey; Bilkent University, UNAM-Institute of Materials Science and Nanotechnology, Ankara, Turkey; Bilkent University, Department of Psychology, Ankara, Turkey; Bilkent University, Aysel Sabuncu Brain Research Center, Ankara, Turkey. Electronic address: .
Źródło:
Neuroscience [Neuroscience] 2016 Oct 15; Vol. 334, pp. 64-75. Date of Electronic Publication: 2016 Jul 28.
Typ publikacji:
Journal Article
Język:
English
Imprint Name(s):
Publication: [New York?] : Elsevier Science
Original Publication: Oxford, Elmsford, N. Y., Pergamon Press
MeSH Terms:
Caloric Restriction*
Aging/*physiology
Cellular Senescence/*physiology
Animals ; Body Weight ; Brain/physiology ; Cell Proliferation/physiology ; Cohort Studies ; Random Allocation ; Telomere/metabolism ; Time Factors ; Zebrafish ; beta-Galactosidase/metabolism
Contributed Indexing:
Keywords: aging; brain; cell proliferation; dietary restriction; telomere; zebrafish
Substance Nomenclature:
EC 3.2.1.23 (beta-Galactosidase)
Entry Date(s):
Date Created: 20160801 Date Completed: 20170912 Latest Revision: 20171116
Update Code:
20240104
DOI:
10.1016/j.neuroscience.2016.07.033
PMID:
27475251
Czasopismo naukowe
Brain 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 (8-8.5months) and old (26-32.5months) 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.
(Copyright © 2016 IBRO. Published by Elsevier Ltd. All rights reserved.)

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