Journal article 654 views 74 downloads
The 5:2 diet does not increase adult hippocampal neurogenesis or enhance spatial memory in mice
EMBO reports, Volume: 24, Issue: 12
Swansea University Authors: Luke Roberts, Amanda K. E. Hornsby , Alanna Thomas, Martina Sassi, Beth David, Jeffrey Davies
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DOI (Published version): 10.15252/embr.202357269
Abstract
New neurones are generated throughout life in the mammalian brain in a process known as adult hippocampal neurogenesis (AHN). Since this phenomenon grants a high degree of neuroplasticity influencing learning and memory, identifying factors that regulate AHN may be important for ameliorating age‐rel...
Published in: | EMBO reports |
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ISSN: | 1469-221X 1469-3178 |
Published: |
Springer Science and Business Media LLC
2023
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Online Access: |
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URI: | https://cronfa.swan.ac.uk/Record/cronfa61550 |
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Abstract: |
New neurones are generated throughout life in the mammalian brain in a process known as adult hippocampal neurogenesis (AHN). Since this phenomenon grants a high degree of neuroplasticity influencing learning and memory, identifying factors that regulate AHN may be important for ameliorating age‐related cognitive decline. Calorie restriction (CR) has been shown to enhance AHN and improve memory, mediated by the stomach hormone, ghrelin. Intermittent fasting (IF), a dietary strategy offering more flexibility than conventional CR, has also been shown to promote aspects of AHN. The 5:2 diet is a popular form of IF; however, its effects on AHN are not well characterised. To address this, we quantified AHN in adolescent and adult wild‐type and ghrelin‐receptor‐deficient mice following 6 weeks on a 5:2 diet. We report an age‐related decline in neurogenic processes. However, the 5:2 diet does not increase AHN nor enhance memory performance, suggesting that this specific form of IF is ineffective in promoting brain plasticity to support learning. |
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Keywords: |
5:2 diet; dietary restriction; ghrelin receptor; intermittent fasting; neurogenesis |
College: |
Faculty of Medicine, Health and Life Sciences |
Funders: |
This project was supported by a grant from the British Society of Neuroendocrinology to LDR, TW and JSD, grants from The Waterloo Foundation (1403/3689, 1403/3758, 1403/4120) and The Rosetrees Trust (A2248) to AKEH, JSD and TW. AKEH and TW wish to acknowledge the generous financial support of the Cardiff University Research Contingency Fund. |
Issue: |
12 |