NAD+ is a coenzyme central to redox metabolism and cellular energy, and its decline with age has made it a focus of research into mitochondrial function.
Nicotinamide adenine dinucleotide (NAD+) is a coenzyme present in all living cells that connects energy production, cellular signalling, and aging. Studies describe NAD+ in two complementary roles: as a redox carrier that shuttles electrons through glycolysis, the tricarboxylic acid cycle, and oxidative phosphorylation, and as a consumed cosubstrate for enzymes including the sirtuins (NAD+-dependent deacylases) and poly(ADP-ribose) polymerases (PARPs) involved in DNA repair.
Because sirtuins regulate mitochondrial biogenesis and metabolic adaptation, NAD+ availability is thought to influence mitochondrial bioenergetics. Research reports that tissue NAD+ levels decline with age in multiple model organisms, attributed to shifts in biosynthetic and consuming enzymes including reduced NAMPT and increased CD38 activity. In preclinical models, supplementation with NAD+ precursors such as nicotinamide mononucleotide (NMN) and nicotinamide riboside (NR) has been reported to raise NAD+ pools, activate sirtuins, and improve markers of mitochondrial and metabolic function in aged rodents. Human clinical findings to date are reported as less consistent than preclinical results.
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