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J Cereb Blood Flow Metab. 2014 Sep;34(9):1440-3. doi: 10.1038/jcbfm.2014.114. Epub 2014 Jul 2.

Caloric restriction impedes age-related decline of mitochondrial function and neuronal activity.

Author information

1
1] Sanders-Brown Center on Aging, University of Kentucky, Lexington, Kentucky, USA [2] Department of Pharmacology and Nutritional Sciences, University of Kentucky, Lexington, Kentucky, USA.
2
1] Magnetic Resonance Research Center, Yale University, New Haven, Connecticut, USA [2] Quantitative Neuroscience with Magnetic Resonance Core Center, Yale University, New Haven, Connecticut, USA [3] Department of Diagnostic Radiology, Yale University, New Haven, Connecticut, USA.
3
1] Magnetic Resonance Research Center, Yale University, New Haven, Connecticut, USA [2] Quantitative Neuroscience with Magnetic Resonance Core Center, Yale University, New Haven, Connecticut, USA [3] Department of Diagnostic Radiology, Yale University, New Haven, Connecticut, USA [4] Department of Biomedical Engineering, Yale University, New Haven, Connecticut, USA.

Abstract

Caloric restriction (CR) prolongs lifespan and retards many detrimental effects of aging, but its effect on brain mitochondrial function and neuronal activity--especially in healthy aging--remains unexplored. Here we measured rates of neuronal glucose oxidation and glutamate-glutamine neurotransmitter cycling in young control, old control (i.e., healthy aging), and old CR rats using in vivo nuclear magnetic resonance spectroscopy. We found that, compared with the young control, neuronal energy production and neurotransmission rates were significantly reduced in healthy aging, but were preserved in old CR rats. The results suggest that CR mitigated the age-related deceleration of brain physiology.

PMID:
24984898
PMCID:
PMC4158670
DOI:
10.1038/jcbfm.2014.114
[Indexed for MEDLINE]
Free PMC Article
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