Coenzyme Q 10 supplementation improves the motor function of middle-aged mice by restoring the neuronal activity of the motor cortex
Physiological aging causes motor function decline and anatomical and biochemical changes in the motor cortex. We confirmed that middle-aged mice at 15-18 months old show motor function decline, which can be restored to the young adult level by supplementing with mitochondrial electron transporter co...
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Published in: | Scientific reports Vol. 13; no. 1; p. 4323 |
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Main Authors: | , , , |
Format: | Journal Article |
Language: | English |
Published: |
England
15-03-2023
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Subjects: | |
Online Access: | Get full text |
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Summary: | Physiological aging causes motor function decline and anatomical and biochemical changes in the motor cortex. We confirmed that middle-aged mice at 15-18 months old show motor function decline, which can be restored to the young adult level by supplementing with mitochondrial electron transporter coenzyme Q
(CoQ
) as a water-soluble nanoformula by drinking water for 1 week. CoQ
supplementation concurrently improved brain mitochondrial respiration but not muscle strength. Notably, we identified an age-related decline in field excitatory postsynaptic potential (fEPSP) amplitude in the pathway from layers II/III to V of the primary motor area of middle-aged mice, which was restored to the young adult level by supplementing with CoQ
for 1 week but not by administering CoQ
acutely to brain slices. Interestingly, CoQ
with high-frequency stimulation induced NMDA receptor-dependent long-term potentiation (LTP) in layer V of the primary motor cortex of middle-aged mice. Importantly, the fEPSP amplitude showed a larger input‒output relationship after CoQ
-dependent LTP expression. These data suggest that CoQ
restores the motor function of middle-aged mice by improving brain mitochondrial function and the basal fEPSP level of the motor cortex, potentially by enhancing synaptic plasticity efficacy. Thus, CoQ
supplementation may ameliorate the age-related decline in motor function in humans. |
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ISSN: | 2045-2322 |