Caloric Restriction Impedes Age-Related Decline of Mitochondrial Function and Neuronal Activity | Zendy

Ai-Ling Lin | Zendy; Daniel Coman | Zendy; Lihong Jiang | Zendy; Douglas L. Rothman | Zendy; Fahmeed Hyder | Zendy

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Caloric Restriction Impedes Age-Related Decline of Mitochondrial Function and Neuronal Activity

Author(s) -

Ai-Ling Lin,

Daniel Coman,

Lihong Jiang,

Douglas L. Rothman,

Fahmeed Hyder

Publication year - 2014

Publication title -

journal of cerebral blood flow and metabolism

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 2.167

H-Index - 193

eISSN - 1559-7016

pISSN - 0271-678X

DOI - 10.1038/jcbfm.2014.114

Subject(s) - glutamate receptor , glutamine , neurotransmission , neurotransmitter , aging brain , caloric theory , brain aging , neuroscience , premovement neuronal activity , mitochondrion , biology , senescence , medicine , endocrinology , dopamine , central nervous system , biochemistry , receptor , cognition , amino acid

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.

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