Among the molecular signatures of aging, few are as consistently measured as the decline of NAD+. Across tissues and species, levels of this central coenzyme drop with age — and because NAD+ sits upstream of both energy metabolism and repair signaling, that decline touches nearly everything.
Two Jobs, One Molecule
NAD+ works first as a redox shuttle — carrying electrons in the reactions that generate ATP — and second as a consumed substrate for signaling enzymes: sirtuins, which regulate metabolism and stress response, and PARPs, which manage DNA repair. The consumption side is key: every sirtuin and PARP reaction destroys an NAD+ molecule.
Why Levels Fall
The research points to a widening gap between synthesis and consumption — salvage pathway enzymes decline while consumers like CD38 and chronically activated PARPs increase. The result is a shrinking budget for both energy and repair.
The Research Toolkit
Laboratories approach the axis from several angles: direct NAD+ supplementation in models, precursor pathway studies, and enzyme-level interventions like NNMT inhibition with 5-Amino-1MQ. Mitochondrial partners MOTS-C and SS-31 complete the shelf in our Anti-Aging collection.
All products discussed are intended strictly for in-vitro research and laboratory use only. They are not for human or veterinary use, consumption, or therapeutic application.
