PUBLICATION
Short-Term Dietary Restriction in Old Zebrafish Changes Cell Senescence Mechanisms
- Authors
- Arslan-Ergul, A., Erbaba, B., Karoglu, E.T., Halim, D.O., Adams, M.
- ID
- ZDB-PUB-160801-1
- Date
- 2016
- Source
- Neuroscience 334: 64-75 (Journal)
- Registered Authors
- Keywords
- Aging, Brain, Cell Proliferation, Dietary Restriction, Telomere, Zebrafish
- MeSH Terms
-
- Aging/physiology*
- Animals
- Body Weight
- Brain/physiology
- Caloric Restriction*
- Cell Proliferation/physiology
- Cellular Senescence/physiology*
- Cohort Studies
- Random Allocation
- Telomere/metabolism
- Time Factors
- Zebrafish
- beta-Galactosidase/metabolism
- PubMed
- 27475251 Full text @ Neuroscience
Citation
Arslan-Ergul, A., Erbaba, B., Karoglu, E.T., Halim, D.O., Adams, M. (2016) Short-Term Dietary Restriction in Old Zebrafish Changes Cell Senescence Mechanisms. Neuroscience. 334:64-75.
Abstract
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 cognitive changes. Advances, which aim to promote better aging are of paramount importance. Dietary restriction is the only non-genetic intervention that reliably extends life- and health-span. Mechanisms of how and why dietary restriction 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 dietary restriction (DR) on actively proliferating cells. We successfully applied a 10 week DR to young and old fish, which resulted in 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.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping