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What is NAD+ used for in research?

Research overview 7 min read

On this page
  1. What is NAD+?
  2. What is NAD+ used for?
  3. NAD+ research areas at a glance
  4. How is NAD+ thought to work?
  5. What kind of studies are these?
  6. Sources

NAD+ (nicotinamide adenine dinucleotide) is a coenzyme that, in research, has mainly been studied as a carrier in the reactions cells use to break down sugars and fats, and as a material several enzyme families use up [G1, G2]. A coenzyme is a helper molecule that enzymes need to run some chemical reactions [G1]. Researchers have also measured NAD+ in different tissues and given NAD+ itself to cells, rats and a small group of people [G3, G6, G7, G8]. NAD+ is a separate molecule from its precursors NR and NMN, so studies that give those precursors are not studies of NAD+ itself [G2, G10].

What is NAD+?

NAD+ is a dinucleotide: two nucleotides, small building-block molecules, joined together. NAD+ takes part in redox reactions, chemical reactions in which electrons pass from one molecule to another [G1]. In some reactions NAD+ picks up electrons and hydrogen and becomes NADH, its reduced form [G2]. NADH then passes them on in other reactions [G2].

Cells can build NAD+ from the amino acid tryptophan or from nicotinic acid [G2]. But most NAD+ is recycled, through what are called salvage pathways, from nicotinamide and related molecules [G2]. NR (nicotinamide riboside) and NMN (nicotinamide mononucleotide) sit on that recycling route: NR is converted to NMN, and NMN to NAD+ [G2]. That is why they are called precursors, molecules a cell turns into NAD+.

What is NAD+ used for?

In research, NAD+ has mainly been studied for its role in cell chemistry [G1, G2]. A few studies have also given NAD+ itself to cells, rats and people [G6–G8]. The research areas, in plain terms:

  • Its job as a coenzyme in the reactions that break down sugars and fats in cells [G2].
  • Its use by enzyme families. Sirtuins, PARPs and CD38 are enzymes, proteins that speed up chemical reactions, and they depend on NAD+ [G1]. PARPs are enzymes involved in DNA repair, and CD38 breaks NAD+ down [G1, G2]. These enzymes use NAD+ up as they work [G2].
  • How much NAD+ tissues hold, and which enzymes make it or break it down, measured in mouse tissues [G3, G4].
  • NAD+ placed outside cells, and whether it gets in, studied in human cell lines and in astrocytes, support cells from the mouse brain [G5, G6].
  • Cells running short of NAD+ after DNA damage, studied in cultured mouse astrocytes [G6].
  • NAD+ itself given to rats in a model of transient focal ischemia, where blood flow to part of the brain is temporarily blocked [G7].
  • NAD+ itself given to people: NAD+ and its breakdown products measured in the blood and urine of 11 healthy men [G8].

A separate body of research gives a precursor, such as NR, and then measures NAD+ [G10]. A 2023 review assessed 25 published human studies of NR [G11].

NAD+ research areas at a glance

Area What researchers looked at Models How strong the evidence is
Cell chemistry NAD+ as a coenzyme in redox reactions, and as the material sirtuins, PARPs and CD38 use up [G2] Summarised across many studies in reviews Established biochemistry, described in reviews
Tissue levels How much NAD+ different tissues hold, and the routes that make it [G3] Mouse tissues Animal tissue measurements
Breakdown by CD38 NAD+ levels and NAD+-breaking activity in mice with and without CD38 [G4] Normal mice and mice lacking CD38 One animal study
NAD+ outside cells Whether NAD+ placed outside cells is broken down first or taken in [G5, G6] Human cell lines; mouse astrocytes Two cell studies, reporting different things
NAD+ and cell death NAD+ levels, mitochondrial changes and cell death after DNA damage, with NAD+ added back [G6] Cultured mouse astrocytes One cell study
NAD+ given to animals Brain NAD+, size of damaged areas and neurological scores [G7] Rat model of interrupted blood flow to the brain One animal study
NAD+ given to people NAD+ and breakdown products in blood and urine, against a saline control [G8] 11 healthy men One small human study; registered studies without posted results [G12]
Precursors (not NAD+) NAD+ measured after NR was given [G10] People and mice Separate literature; 25 human NR studies per one review [G11]

Evidence levels describe the study types in the sources listed; they are not a grading by the sources' authors.

How is NAD+ thought to work?

A carrier in sugar and fat breakdown. In glycolysis (the breakdown of glucose), fatty-acid oxidation and the TCA cycle, a loop of follow-on reactions, NAD+ is reduced to NADH [G2]. NADH then drives the production of ATP, the molecule cells use to run most of their reactions, in mitochondria, small compartments inside the cell [G2].

Made, used up, recycled. Sirtuins, PARPs, CD38 and SARM1 split NAD+ into nicotinamide and ADP-ribose, and nicotinamide is recycled into NAD+ [G2]. Mori et al., Aksoy et al. and Nikiforov et al. write "NAD", without the plus, and their findings are reported that way here [G3–G5]. In mouse tissues, Mori et al. found NAD levels highest in liver, kidney, heart and skeletal muscle, and much lower in blood, with the route through NMN predominating [G3]. In mice lacking CD38, Aksoy et al. found higher tissue NAD levels than in normal mice [G4]. In most tissues of the CD38-deficient mice, NAD-breaking activity in the cell's outer membrane, mitochondria, nuclei and sarcoplasmic reticulum (an internal membrane network in muscle cells) was "essentially absent" [G4]. They called CD38 "a major regulator of cellular NAD levels" [G4].

PARP-1 and running short. Alano et al. exposed cultured mouse astrocytes to DNA-damaging chemicals that over-activate PARP-1 [G6]. Before the cells died, NAD+ ran low, the mitochondria lost membrane potential (the electrical charge across their membrane), and mitochondrial permeability transition (MPT), an opening up of that membrane, occurred [G6]. When NAD+ was added back to the cells, the authors reported that membrane potential recovered and that MPT and cell death were blocked [G6].

Ying et al. used that idea as the rationale for a rat study [G7]. NAD+ itself, given in the transient focal ischemia model, raised brain NAD+ content [G7]. The NAD+ group had smaller infarcts, areas of damaged tissue, and lower neurological deficit scores [G7]. Rats given nicotinamide the same way and in the same amount did not show smaller infarcts [G7].

Getting into cells, or not. The cell studies differ. In human cell lines, Nikiforov et al. reported that nucleotides such as NAD and NMN were broken down outside the cells into smaller molecules that can enter, and those were converted to NAD inside [G5]. In mouse astrocytes, Alano et al. stated that "extracellular NAD+ can raise intracellular NAD+ concentrations" [G6]. Xie et al. describe uptake of intact NAD+ into mammalian mitochondria as controversial, with no mammalian NAD+ transporter "discovered so far" [G2].

In the human study, researchers measured NAD+ and its breakdown products (nicotinamide, methylnicotinamide, ADP-ribose and NMN) in plasma and urine, against a saline control group [G8].

The authors read their blood and urine measurements as "consistent with NAD+ glycohydrolase and NAD+ pyrophosphatase activity", enzymes that break NAD+ down outside cells [G8].

What kind of studies are these?

Cell studies test a molecule on cells in a dish. Animal studies test it in a living animal. Human studies test it in people.

Most sources in this overview are reviews, tissue measurements, and cell or animal studies [G1–G7]. Only one study in this overview gave NAD+ itself to people: 11 healthy men, randomised to NAD+ (8 men) or a saline control (3 men), with blood and urine measured [G8].

The study's funding statement lists a private NAD+ research company, and two authors declared ties to it [G8].

A search of the ClinicalTrials.gov registry in October 2026 found registered studies of NAD+ itself, none with results posted on the registry [G12].

See also the same kind of research overview for KPV. Back to the Limitless Science home page.

Sources

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