NAD+ in Longevity Research
Sirtuin substrate biology and emerging redox studies.
- 1NAD+ is the rate-limiting substrate for sirtuins and PARPs.
- 2Tissue NAD+ declines with age in every mammalian species studied.
- 3Precursor supplementation (NR, NMN) raises tissue NAD+ in humans.
- 4Direct NAD+ work allows acute pathway saturation studies.
Why NAD+ Matters
Nicotinamide adenine dinucleotide (NAD+) is a redox cofactor present in every living cell. Beyond its role in electron transport, NAD+ is the obligate substrate for sirtuins (SIRT1-7) and PARPs — enzymes that govern DNA repair, mitochondrial biogenesis, and chromatin state.
Age-Related Decline
Tissue NAD+ falls with age across mammals studied. The decline tracks with sirtuin activity loss, increased DNA damage signaling, and mitochondrial dysfunction — three classic hallmarks of aging.
Precursor vs. Direct NAD+ Research
Most clinical work has focused on precursors (NR, NMN) because of oral bioavailability. Direct NAD+ research peptides and infusions are used in laboratory settings to bypass precursor metabolism and test acute pathway saturation effects.
