NR induces PGC-1α-associated energy metabolism genes

Because the treatment of NR promotes PGC-1α expression and increases intracellular NAD+ levels, it is interesting to know whether the PGC-1α associated energy metabolism genes were affected by the NR treatments. Because it has been reported that some of these genes were downregulated in the AD brain, we tested the messenger RNA (mRNA) levels of these genes in the brain extract from Tg2576 mice. We found that treating Tg2576 mice with NR for 3 months significantly promoted the expression of gene products involved in a wide range of mitochondrial metabolism, such as citrate synthase (Fig. 7A) and aconitase genes (Fig. 7B) in the tricarboxylic acid cycle; pyruvate dehydrogenase kinase (Fig. 7E) in pyruvate metabolism, cytochrome c subunit Vic in mitochondrial oxidative-phosphorylation (Fig. 7F); the human phosphoglycerate kinase and glucose phosphate isomerase 1 genes in glycolysis (Fig. 7G), assessed by quantitative RT-PCR suggesting that NR might promote cognitive performance, in part, by inducing expression of gene products involved in mitochondrial energy metabolism and linked with PGC-1α expression.