NAD+ serves as a required co-substrate for the sirtuin family of enzymes (SIRT1-7), which regulate gene expression, DNA repair, and mitochondrial function. Sirtuins cannot function without NAD+ — as NAD+ levels decline with age, sirtuin activity decreases proportionally. This relationship has made NAD+ a focal point of aging biology research.1
Studies in aging mouse models have shown that boosting NAD+ levels through supplementation with precursors (NMN and NR) restored sirtuin activity and improved markers of metabolic health, mitochondrial function, and DNA repair in aged tissues. A landmark 2013 study by Gomes et al. in Cell demonstrated that raising NAD+ levels in aged mice restored mitochondrial function in skeletal muscle to levels comparable to young mice.2






