NAD+ is synthesized from tryptophan and vitamin B3 precursors, consumed by sirtuins and PARPs, and regenerated via the salvage pathway.
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NAD+ Lifecycle and Salvage
NAD+ (oxidized)
NADH (carries electrons)
Sirtuins (longevity enzymes)
NMN / NR precursors
→
Electron transfer
NAD+ (nicotinamide adenine dinucleotide) is both an electron carrier in cellular respiration and a substrate consumed by enzymes that regulate aging, DNA repair, and metabolism. Unlike ATP, which is recycled thousands of times per second, NAD+ is a limiting resource that can be depleted faster than it is replenished.
The salvage pathway is the dominant route in most cells. NAMPT converts nicotinamide to NMN, NMN is converted to NAD+, and the cycle continues. NMN and NR supplements both enter this pathway and are widely studied for their ability to raise tissue NAD+ levels, which decline 40-50% between young adulthood and old age.
Sirtuins (SIRT1-7) use NAD+ to deacetylate proteins and histones, turning off pro-aging gene programs and promoting mitochondrial biogenesis. Each deacetylation reaction destroys one NAD+ molecule, linking gene regulation directly to metabolic status.
PARPs consume NAD+ at very high rates in response to DNA strand breaks. Oxidative stress or genotoxic exposure can trigger PARP hyperactivation, draining the cellular NAD+ pool rapidly. CD38, an ectoenzyme upregulated in aging and inflammation, is a major driver of age-related NAD+ decline and consumes more NAD+ than all sirtuins combined.
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Source & accuracy
This nad+ lifecycle and salvage is an editorial illustration built to represent the concept accurately. Where it shows figures, they are typical or representative values chosen to make the relationship clear, not a single underlying dataset. The diagram and its explainer are reviewed and maintained centrally, and updated over time as understanding improves.
How cells build and rebuild NAD+
NAD+ can be made by several routes. The de novo pathway starts from the amino acid tryptophan; other routes use the vitamin B3 forms nicotinic acid (the Preiss-Handler pathway) and nicotinamide. Most day-to-day turnover, however, runs through the salvage pathway, which recycles nicotinamide released when NAD+-consuming enzymes do their work.
In the salvage pathway, the enzyme NAMPT converts nicotinamide to nicotinamide mononucleotide (NMN), and NMNAT enzymes then add an adenylyl group to form NAD+. NAMPT is generally considered the rate-limiting step, which is why it is a focus of metabolic research.
Producers, consumers, and turnover
NAD+ is not stored in large amounts; it is continuously consumed and regenerated. Sirtuins use it to deacetylate proteins, PARPs use it during DNA repair, and CD38 consumes it in immune signaling, each releasing nicotinamide that the salvage pathway feeds back into the cycle.
Precursors marketed for raising NAD+, such as nicotinamide riboside and NMN, enter through these same pathways. Their long-term effects in humans remain under study. This is general educational content on metabolism, not medical or supplement advice; consult a qualified professional.
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