ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2009
Transgenic mice expressing the Nmnat1 protein manifest robust delay in axonal degeneration in vivo.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2009. 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 93 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
93 citing papers in PubMed, 154 citations in OpenAlex.
- Nicotinamide Mononucleotide Adenylyltransferase 1 and NADMetabolites · 2026Review
- Programmed axon degeneration: mechanism, inhibition and therapeutic potential.Nature reviews. Neuroscience · 2026Review
- Near infrared fluorophore specific for annexin A2 identifies peripheral nerve injury in a rodent transection model.Frontiers in cell and developmental biology · 2026Article
- Bridging the Gap: Contemporary Paradigms in Nerve Scaffolds and Regeneration.Advances in wound care · 2025Review
- Identification and characterization ofClinical case reports · 2024Article
- Messenger RNA transport on lysosomal vesicles maintains axonal mitochondrial homeostasis and prevents axonal degeneration.Nature neuroscience · 2024Article
- Article
- A nerve-wracking buzz: lessons fromFrontiers in aging neuroscience · 2023Review
- Clinical features and genetic spectrum of NMNAT1-associated retinal degeneration.Eye (London, England) · 2022Article
- Alpha-synucleinopathy reduces NMNAT3 protein levels and neurite formation that can be rescued by targeting the NAD+ pathway.Human molecular genetics · 2022Article
- Balancing NADCellular and molecular life sciences : CMLS · 2022Review
- Coordinated NADPH oxidase/hydrogen peroxide functions regulate cutaneous sensory axon de- and regeneration.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- NADInternational journal of molecular sciences · 2022Article
- NMNAT2 is downregulated in glaucomatous RGCs, and RGC-specific gene therapy rescues neurodegeneration and visual function.Molecular therapy : the journal of the American Society of Gene Therapy · 2022Article
- The Putative Drosophila TMEM184B Ortholog Tmep Ensures Proper Locomotion by Restraining Ectopic Firing at the Neuromuscular Junction.Molecular neurobiology · 2022Article
- Lessons from Injury: How Nerve Injury Studies Reveal Basic Biological Mechanisms and Therapeutic Opportunities for Peripheral Nerve Diseases.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2021Review
- Review
- A Novel NAD Signaling Mechanism in Axon Degeneration and its Relationship to Innate Immunity.Frontiers in molecular biosciences · 2021Review
- Dual Specificity Phosphatases Support Axon Plasticity and Viability.Molecular neurobiology · 2021Article
- The NADNature · 2020Article
33 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
4 authors at 2 institutions in 1 country.
Funding
Abstract
Axonal degeneration is a key component of a variety of neurological diseases. Studies using wld(s) mutant mice have demonstrated that delaying axonal degeneration slows disease course and prolongs survival in neurodegenerative disease models. The Wld(s) protein is normally localized to the nucleus, and contains the N terminus of ubiquitination factor Ube4b fused to full-length Nmnat1, an NAD biosynthetic enzyme. While Nmnat enzymatic activity is necessary for Wld(s)-mediated axonal protection, several important questions remain including whether the Ube4b component of Wld(s) also plays a role, and in which cellular compartment (nucleus vs cytosol) the axonal protective effects of Nmnat activity are mediated. While Nmnat alone is clearly sufficient to delay axonal degeneration in cultured neurons, we sought to determine whether it was also sufficient to promote axonal protection in vivo. Using cytNmnat1, an engineered mutant of Nmnat1 localized only to the cytoplasm and axon, that provides more potent axonal protection than that afforded by Wld(s) or Nmnat1, we generated transgenic mice using the prion protein promoter (PrP). The sciatic nerve of these cytNmnat1 transgenic mice was transected, and microscopic analysis of the distal nerve segment 7 d later revealed no evidence of axonal loss or myelin debris, indicating that Nmnat alone, without any other Wld(s) sequences, is all that is required to delay axonal degeneration in vivo. These results highlight the importance of understanding the mechanism of Nmnat-mediated axonal protection for the development of new treatment strategies for neurological disorders.
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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.