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A recent study confirms the central role of NAD+ in relation to ageing

2026-03-24

A recent study highlights the key role of NAD+ in cellular energy, metabolism and ageing. It sheds valuable light on the value of strategies aimed at preserving its availability at the heart of cells.

NAD+ and its relationship with ageing

What is NAD+ and why is it essential to cells?

NAD+ (nicotinamide adenine dinucleotide) is an essential coenzyme present in every cell of the body.

It plays a central role in many fundamental biological reactions, particularly those linked to energy production and cell regulation.

In biological terms, NAD+ is involved in:

  • the oxidation-reduction reactions needed to produce ATP in the mitochondria
  • the metabolism of nutrients (carbohydrates, lipids, amino acids)
  • activation of enzymes involved in DNA repair and cell signalling
  • maintaining cell balance in the face of metabolic aggression

NAD+ levels decline progressively with ageing (1), but also in situations of metabolic stress, chronic inflammation or high energy demand.

The role of NAD+ in cellular ageing: what does the study reveal?

A recent scientific review summarises the major advances in NAD+ metabolism and its involvement in ageing and age-related diseases (2).

NAD+ and mitochondrial energy production

The authors point out that NAD+ plays a central role in cell function, notably through its role in mitochondrial function.

Mitochondria, which are responsible for energy production, are closely dependent on the availability of NAD+ to maintain their efficiency and integrity.

The review shows that the progressive decrease in NAD+ with age is associated with an alteration in mitochondrial health, now considered to be an important marker of cellular ageing.

NAD+ is essential for the reactions that enable ATP to be produced, and directly conditions the energy capacity of cells.

When its availability decreases, mitochondria become less efficient, leading to a drop in energy production and reduced recovery from physiological stresses.

NAD+ and the maintenance of mitochondrial homeostasis

In addition to energy production, the review highlights the role of NAD+ in several mechanisms essential to the maintenance of mitochondrial homeostasis, in particular:

  • mitophagy, which enables the elimination of damaged mitochondria
  • the response to misfolded proteins, essential for preserving cellular function
  • support for antioxidant systems

The progressive dysfunction of these mechanisms contributes to the accumulation of cellular damage observed during ageing.

NAD+, oxidative stress and cell repair

The authors also highlight the link between NAD+ and the ability of cells to cope with oxidative stress.

By participating in the activation of certain enzymes involved in DNA repair and cellular regulation, NAD+ contributes indirectly to the preservation of cellular integrity.

The progressive decrease in NAD+ with age is associated with a loss of efficiency in repair systems and greater vulnerability to oxidative stress, two phenomena considered to be major components of the cellular ageing process.

A major biological target in ageing and age-related diseases

The review also points out that a drop in NAD+ is observed in several conditions associated with ageing, such as cognitive decline, sarcopenia (loss of muscle mass) and certain metabolic diseases (insulin resistance, chronic inflammation, etc.).

These conditions have one thing in common: an alteration in mitochondrial health.

This convergence provides a better understanding of why NAD+ is now seen as a central hub in cellular ageing.

And it explains the growing interest in approaches aimed at supporting NAD+ metabolism.

How (and when) should NAD+ supplementation be considered?

It's important to remember that lifestyle has a major influence on cell metabolism and NAD+ demand: diet, physical activity, sleep quality and stress management all play a decisive role in cell energy balance.

Supplementation should above all complement these essential factors, as part of an overall approach aimed at supporting cellular function.

Opt for NAD+ precursors

As NAD+ is an unstable and poorly bioavailable molecule when taken orally, the focus is on its precursors, which the body can convert naturally into NAD+ at the cellular level.

The most widely studied NAD+ precursors include:

  • NMN (nicotinamide mononucleotide)
  • NR (nicotinamide riboside) (3)

These intermediate molecules are used by cells as metabolic substrates to support NAD+ synthesis, depending on physiological needs.

-Discover Nicotinamide Mononucleotide, a direct precursor of NAD+ involved in cellular metabolic pathways.

-Discover NMN Max, a concentrated NMN formula designed to support endogenous NAD+ synthesis mechanisms.

-Discover Nicotinamide Riboside Chloride, a dietary supplement containing nicotinamide riboside chloride (a vitamin B3 derivative).

Towards synergistic approaches?

Research is also looking at combined approaches and synergistic formulas, combining several nutrients involved in NAD+ metabolism.

Among the ingredients studied for their interaction with certain NAD+ regulatory pathways are:

  • apigenin: a flavonoid naturally present in some plants, studied for its potential ability to modulate the activity of enzymes involved in NAD+ degradation (4)
  • BluNAD Booster™: an innovative plant combination, explored for its interaction with these same regulatory pathways, and its potential role in maintaining cellular availability of NAD+

-Discover NAD+ Booster Formula, a synergistic formula combining several NAD+ precursors and cofactors (nicotinamide riboside, apigenin and BluNAD Booster™).

SUPERSMART ADVICE

References

  1. Camacho-Pereira J, Tarragó MG, Chini CCS, Nin V, Escande C, Warner GM, Puranik AS, Schoon RA, Reid JM, Galina A, Chini EN. CD38 Dictates Age-Related NAD Decline and Mitochondrial Dysfunction through an SIRT3-Dependent Mechanism. Cell Metab. 2016 Jun 14;23(6):1127-1139. doi: 10.1016/j.cmet.2016.05.006. PMID: 27304511; PMCID: PMC4911708.
  2. Yusri K, Jose S, Vermeulen KS, Tan TCM, Sorrentino V. The role of NAD+ metabolism and its modulation of mitochondria in aging and disease. NPJ Metab Health Dis. 2025 Jun 18;3(1):26. doi: 10.1038/s44324-025-00067-0. PMID: 40604314; PMCID: PMC12177089.
  3. Yoshino J, Baur JA, Imai SI. NAD+Intermediates: The Biology and Therapeutic Potential of NMN and NR. Cell Metab. 2018 Mar 6;27(3):513-528. doi: 10.1016/j.cmet.2017.11.002. Epub 2017 Dec 14. PMID: 29249689; PMCID: PMC5842119.
  4. Escande C, Nin V, Price NL, Capellini V, Gomes AP, Barbosa MT, O'Neil L, White TA, Sinclair DA, Chini EN. Flavonoid apigenin is an inhibitor of the NAD+ ase CD38: implications for cellular NAD+ metabolism, protein acetylation, and treatment of metabolic syndrome. Diabetes. 2013 Apr;62(4):1084-93. doi: 10.2337/db12-1139. Epub 2012 Nov 19. PMID: 23172919; PMCID: PMC3609577.

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