Journal
APPLIED PHYSIOLOGY NUTRITION AND METABOLISM
Volume 48, Issue 5, Pages 393-402Publisher
CANADIAN SCIENCE PUBLISHING
DOI: 10.1139/apnm-2022-0111
Keywords
Key words; folic acid; apoptosis; telomere; oxidative damage; neural stem cell; senescence-accelerated mouse prone 8 (SAMP8)
Categories
Ask authors/readers for more resources
Folic acid supplementation can improve cognitive performance and inhibit neural stem cell apoptosis in the aging brain. However, its role in age-associated telomere attrition is still unclear.
Folic acid (FA) could improve cognitive performance and attenuate brain cell injury in the aging brain; FA supplementation is also associated with inhibiting neural stem cell (NSC) apoptosis. However, its role in age-associated telomere attrition remains unclear. We hypothesized that FA supplementation attenuates age-associated apoptosis of NSCs in mice via alleviating telomere attrition in senescence-accelerated mouse prone 8 (SAMP8). In this study, 4-month-old male SAMP8 mice were assigned equal numbers to four different diet groups (n = 15). Fifteen age-matched senescence-accelerated mouse resistant 1 mice, fed with the FA-normal diet, were used as the standard aging control group. After FA treatment for 6 months, all mice were sacrificed. NSC apoptosis, proliferation, oxidative damage, and telomere length were evaluated by immunofluorescence and Q-fluorescent in situ hybridization. The results showed that FA supplementation inhibited age-associated NSC apoptosis and prevented telomere attrition in the cerebral cortex of SAMP8 mice. Importantly, this effect might be explained by the decreased levels of oxidative damage. In conclusion, we demonstrate it may be one of the mechanisms by which FA inhibits age-associated NSC apoptosis by alleviating telomere length shortening.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available