ArticleCell death and differentiation2015
A rise in NAD precursor nicotinamide mononucleotide (NMN) after injury promotes axon degeneration.
Article in Cell death and differentiation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03642990 (Nicotinamide Riboside), which is not on this map. Cited by 156 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Nicotinamide Riboside (NR) in Paclitaxel-induced Peripheral Neuropathy
Who cites it
156 citing papers in PubMed, 259 citations in OpenAlex.
- Nicotinamide mononucleotide supplementation enhances aerobic capacity in amateur runners: a randomized, double-blind study.Journal of the International Society of Sports Nutrition · 2021Trial
- Direct activation of SARM1 by dsDNA is not supported by biochemical and cellular evidence.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Review
- Peripheral Neuropathy in Metabolic Stress.International journal of molecular sciences · 2026Review
- Boldine inhibits SARM1 NADase Activity and Preserves Axonal Integrity After Nerve Injury.bioRxiv : the preprint server for biology · 2026Article
- The rise and fall of SARM1 base-exchange inhibitors.Communications chemistry · 2026Article
- SARM1 activation promotes axonal degeneration via a two-step phase transition.Nature chemical biology · 2026Article
- Preliminary exploration of acute limit toxicity testing for nicotinamide mononucleotide in the neonatal population.Frontiers in pharmacology · 2026Article
- Precision Nanodelivery Enables Spatiotemporal Control of NAD⁺ Metabolism in Ageing and Disease.International journal of nanomedicine · 2026Review
- Programmed axon degeneration: mechanism, inhibition and therapeutic potential.Nature reviews. Neuroscience · 2026Review
- CD38-NAD(+) Axis: New Insights into Glaucoma Therapy.Molecular neurobiology · 2025Review
- A redox-dependent switch governing sensory axon degeneration and regeneration.Scientific reports · 2025Article
- Cancer cell death induced by the NAD antimetabolite Vacor discloses the antitumor potential of SARM1.FEBS letters · 2025Article
- Nicotinamide riboside and nicotinamide mononucleotide facilitate NADScience advances · 2025Article
- Free Vastus Lateralis Functional Muscle Transfer: An Approach to Facial Reanimation and Reconstruction in Radical Parotidectomy.Plastic and reconstructive surgery. Global open · 2025Article
- Programmed neurite degeneration in human central nervous system neurons driven by changes in NADCell death & disease · 2025Article
- Gap junction intercellular communications regulates activation of SARM1 and protects against axonal degeneration.Cell death & disease · 2025Article
- Review
- Research advances in the function and anti-aging effects of nicotinamide mononucleotide.Journal of Zhejiang University. Science. B · 2024Review
- Nicotinamide Adenine Dinucleotide Precursor Supplementation Modulates Neurite Complexity and Survival in Motor Neurons from Amyotrophic Lateral Sclerosis Models.Antioxidants & redox signaling · 2024Article
96 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
23 authors at 7 institutions in 3 countries.
Funding
Abstract
NAD metabolism regulates diverse biological processes, including ageing, circadian rhythm and axon survival. Axons depend on the activity of the central enzyme in NAD biosynthesis, nicotinamide mononucleotide adenylyltransferase 2 (NMNAT2), for their maintenance and degenerate rapidly when this activity is lost. However, whether axon survival is regulated by the supply of NAD or by another action of this enzyme remains unclear. Here we show that the nucleotide precursor of NAD, nicotinamide mononucleotide (NMN), accumulates after nerve injury and promotes axon degeneration. Inhibitors of NMN-synthesising enzyme NAMPT confer robust morphological and functional protection of injured axons and synapses despite lowering NAD. Exogenous NMN abolishes this protection, suggesting that NMN accumulation within axons after NMNAT2 degradation could promote degeneration. Ectopic expression of NMN deamidase, a bacterial NMN-scavenging enzyme, prolongs survival of injured axons, providing genetic evidence to support such a mechanism. NMN rises prior to degeneration and both the NAMPT inhibitor FK866 and the axon protective protein Wld(S) prevent this rise. These data indicate that the mechanism by which NMNAT and the related Wld(S) protein promote axon survival is by limiting NMN accumulation. They indicate a novel physiological function for NMN in mammals and reveal an unexpected link between new strategies for cancer chemotherapy and the treatment of axonopathies.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.