TY - JOUR
T1 - Coenzyme Q10 supplementation reverses age-related impairments in spatial learning and lowers protein oxidation
AU - Shetty, Ritu A.
AU - Forster, Michael J.
AU - Sumien, Nathalie
N1 - Funding Information:
Acknowledgments This research was supported by the grants R01 AG27353 and AG22550 from the National Institutes of Health and the National Institute on Aging. The authors also wish to thank Tishcon Corp. (Westbury, NY) for providing with CoQ for this study.
PY - 2013/10
Y1 - 2013/10
N2 - Coenzyme Q10 (CoQ) is widely available as a dietary supplement and remains under consideration as a treatment for age-associated neurodegenerative conditions. However, no studies have determined if supplementation, initiated relatively late in life, could have beneficial effects on mild functional impairments associated with normal brain aging. Accordingly, the current study assessed the effect of CoQ intake in older mice for which cognitive and psychomotor impairments were already evident. Separate groups of young (3.5 months) and relatively old mice (17.5 months) were fed a control diet or a diet supplemented with low (0.72 mg/g) or high (2.81 mg/g) concentrations of CoQ for 15 weeks. After 6 weeks, the mice were given tests for spatial learning (Morris water maze), spontaneous locomotor activity, motor coordination, and startle reflex. Age-related impairments in cognitive and psychomotor functions were evident in the 17.5-month-old mice fed the control diet, and the low-CoQ diet failed to affect any aspect of the impaired performance. However, in theMorris water maze test, old mice on the high-CoQ diet swam to the safe platform with greater efficiency than the mice on the control diet. The old mice supplemented with the high- CoQ diet did not show improvement when spatial performance was measured using probe trials and failed to show improvement in other tests of behavioral performance. Protein oxidative damage was decreased in the mitochondria fromthe heart, liver, and skeletalmuscle of the high-CoQ-supplementedmice and, to some extent, in the brain mitochondria. Contrasting with the deleterious effect of long-term CoQ supplementation initiated during young adulthood previously published, this study suggests that CoQ improves spatial learning and attenuates oxidative damage when administered in relatively high doses and delayed until early senescence, after agerelated declines have occurred. Thus, in individuals with age-associated symptoms of cognitive decline, high- CoQ intake may be beneficial.
AB - Coenzyme Q10 (CoQ) is widely available as a dietary supplement and remains under consideration as a treatment for age-associated neurodegenerative conditions. However, no studies have determined if supplementation, initiated relatively late in life, could have beneficial effects on mild functional impairments associated with normal brain aging. Accordingly, the current study assessed the effect of CoQ intake in older mice for which cognitive and psychomotor impairments were already evident. Separate groups of young (3.5 months) and relatively old mice (17.5 months) were fed a control diet or a diet supplemented with low (0.72 mg/g) or high (2.81 mg/g) concentrations of CoQ for 15 weeks. After 6 weeks, the mice were given tests for spatial learning (Morris water maze), spontaneous locomotor activity, motor coordination, and startle reflex. Age-related impairments in cognitive and psychomotor functions were evident in the 17.5-month-old mice fed the control diet, and the low-CoQ diet failed to affect any aspect of the impaired performance. However, in theMorris water maze test, old mice on the high-CoQ diet swam to the safe platform with greater efficiency than the mice on the control diet. The old mice supplemented with the high- CoQ diet did not show improvement when spatial performance was measured using probe trials and failed to show improvement in other tests of behavioral performance. Protein oxidative damage was decreased in the mitochondria fromthe heart, liver, and skeletalmuscle of the high-CoQ-supplementedmice and, to some extent, in the brain mitochondria. Contrasting with the deleterious effect of long-term CoQ supplementation initiated during young adulthood previously published, this study suggests that CoQ improves spatial learning and attenuates oxidative damage when administered in relatively high doses and delayed until early senescence, after agerelated declines have occurred. Thus, in individuals with age-associated symptoms of cognitive decline, high- CoQ intake may be beneficial.
KW - Aging
KW - C57BL/6J
KW - CoenzymeQ
KW - Mitochondria
KW - Oxidative damage
KW - Ubidecarenone
KW - Ubiquinone
UR - http://www.scopus.com/inward/record.url?scp=84892614039&partnerID=8YFLogxK
U2 - 10.1007/s11357-012-9484-9
DO - 10.1007/s11357-012-9484-9
M3 - Article
C2 - 23138632
AN - SCOPUS:84892614039
SN - 0161-9152
VL - 35
SP - 1821
EP - 1834
JO - Age
JF - Age
IS - 5
ER -