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It is known that NAD+ levels in the human body gradually decrease with age, which directly or indirectly affects many cellular processes, including energy metabolism, chromosome stability, DNA repair, and immune cell activity. Therefore, restoring NAD+ levels to alleviate aging is the goal of many anti-aging studies. In this case, NMN and NR have been attracting attention as precursors of NAD+ biosynthesis.
Recently, a research team has linked NAD+ to twelve "markers of aging" and integrated multiple studies on aging-related pathways and conditions affected by NAD+ precursors NMN and NR.
Research Model: Worm
Aging-related pathways and conditions: Activate sirtuins, which in turn deacetylate and trigger the transcription factors PGG-1α, FOXO and other aging-related factors.
Research Model: Worm
Aging-Related Pathways and Conditions: Restores muscle, melanocyte stem cell pool, and neuronal function by activating UPRmt and inhibiting protein synthesis.
Research models: worms, mice, yeast
Aging-Related Pathways and Conditions: Activation of UPRmt, leading to translocation of FOXO transcription factors, triggers antioxidant defenses in worms and mice, and delays lifespan and health. Triggering of UPRmt has also been observed in yeast models.
In mice, NR treatment increased NAD+ levels, and PGC-1α-mediated degradation of Bace1 resulted in reduced Aβ production.
Research models: mice, worms
Aging-Related Pathways and Conditions: NR treatment suppresses high-fat DIO by stimulating Sirt1 activity and increasing NAD+ levels.
NMN potentiates glucose intolerance in diabetic mouse models and increases hepatic insulin sensitivity or by restoring NAD+ levels.
NR/NMN in high-fat diet-fed mice increased the use of lipids as substrates, improved insulin sensitivity, and increased energy expenditure.
Research model: HEK293 cells, rat
Aging-Related Pathways and Conditions: Suppresses noise-induced hearing loss and leads to NAD+-dependent Sirt3 activity-mediated neurite ganglion regeneration. NAD+-directed Sirt1 activity levels increase and slow axonal degeneration.
Research model: mouse
Aging-Related Pathways and Conditions: Reducing senescence of neurons and melanocyte stem cells. Enhanced mitochondrial function, dependent on Sirt1 function.
Research models: mice, WRN-KD cells, worms
Aging-Related Pathways and Conditions: Accelerated aging in Werner syndrome is mediated by impaired mitochondrial function and mitophagy, and increasing cellular NAD+ levels stabilizes the Werner syndrome phenotype.
NAD+ supplementation helps restore NAD+ metabolic profiles and enhance mitochondrial quality through DCT-1 and ULK-1-dependent mitophagy.
Research models: BMMC, mice
Aging-Related Pathways and Conditions: Significant reduction of IgE-mediated allergic reactions.
Suppresses mast cell degranulation and allergic responses, but Sirt6 is required for these improvements.
Research demonstrates that NAD+ precursors promote healthy aging and delay the onset of many age-related diseases.
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[1] Rahman SU, Qadeer A, Wu Z. Role and Potential Mechanisms of Nicotinamide Mononucleotide in Aging. Aging Dis. 2024 Apr 1;15(2):565-583. doi: 10.14336/AD.2023.0519-1. PMID: 37548938; PMCID: PMC10917541.
*Special note - This article is for informational purposes only and cannot replace a doctor's treatment diagnosis and advice. It should not be regarded as a recommendation or proof of efficacy of the medical products involved. If it involves disease diagnosis, treatment, and rehabilitation, please be sure to go to a professional medical institution to seek professional advice.
