Folic acid delays age-related cognitive decline in senescence-accelerated mouse prone 8: alleviating telomere attrition as a
potential mechanism
Figure 4.FA supplementation protected against telomeric DNA oxidation and telomere length shortening in brain of SAMP8 mice. Mice were assigned to treatment groups as described in Figure 1. (A) Level of 8-hydroxy-2'-deoxyguanosine (8-OHdG) in genomic DNA quantified by ELISA [F(5,54) = 75.370, P<0.001]. (B) Level of telomeric DNA oxidation quantified by qPCR [F(5,54) = 70.139, P<0.001]. (C) Telomere length quantified by qPCR [F(5,54) = 24.184, P<0.001]. (D) Representative telomere Q-FISH images in neurons (blue DAPI-stained nuclei; red telomeric probe; green NeuN-stained neuron). Neuronal telomere length quantified by Q-FISH in cerebral cortex [F(5,24) = 54.582, P<0.001] (E) and hippocampal CA1 region [F(5,24) = 68.765, P<0.001] (F). Scale bar = 10 μm. Data are expressed as mean ± SD (n=10 mice/group for ELISA and qPCR assays, n=5 mice/group for Q-FISH assay). *P<0.05 compared with FA-N group. #P<0.05 compared with Con-Y group. &P<0.05 compared between FA-L and FA-H groups.