Low levels of NMNAT2 compromise axon development and survival
Open accessAbstract
Nicotinamide mononucleotide adenylyltransferase 2 (NMNAT2) is an endogenous axon maintenance factor that preserves axon health by blocking Wallerian-like axon degeneration. Mice lacking NMNAT2 die at birth with severe axon defects in both the peripheral nervous system and central nervous system so the complete absence of NMNAT2 in humans is likely to be similarly harmful but probably rare. However, there is evidence of widespread natural variation in human NMNAT2 mRNA expression so it is important to establish whether reduced levels of NMNAT2 have consequences that impact health. While mice that express reduced levels of NMNAT2, either those heterozygous for a silenced Nmnat2 allele or compound heterozygous for one silenced and one partially silenced Nmnat2 allele, remain overtly normal into old age, we now report that Nmnat2 compound heterozygote mice present with early and age-dependent peripheral nerve axon defects. Compound heterozygote mice already have reduced numbers of myelinated sensory axons at 1.5 months and lose more axons, likely motor axons, between 18 and 24 months and, crucially, these changes correlate with early temperature insensitivity and a later-onset decline in motor performance. Slower neurite outgrowth and increased sensitivity to axonal stress are also evident in primary cultures of Nmnat2 compound heterozygote superior cervical ganglion neurons. These data reveal that reducing NMNAT2 levels below a particular threshold compromises the development of peripheral axons and increases their vulnerability to stresses. We discuss the implications for human neurological phenotypes where axons are longer and have to be maintained over a much longer lifespan.
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NMNAT2 is enriched in brain, and adequate levels appear essential for axon development and survival.
“While NMNAT1 and NMNAT3 are ubiquitously expressed, NMNAT2 is enriched in the brain, and adequate levels of NMNAT2 seem to be essential for axon development and survival (Gilley et al., 2019).”
From NAD+ in Brain Aging and Neurodegenerative Disorders (2019) · cites this paper as Gilley et al., 2019
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Cites
Analysis of protein-coding genetic variation in 60,706 humans
Exome Aggregation Consortium, Lek, M., Karczewski, K. J., Minikel, E. V., Samocha, K. E., Banks, E., Fennell, T., O’Donnell-Luria, A. H., Ware, J. S., Hill, A. J., et al. (2016) · Nature · doi:10.1038/nature19057 · Cited by 9,587 · see citing works
Nociceptors: the sensors of the pain pathway
Dubin, A. E., & Patapoutian, A. (2010) · Journal of Clinical Investigation · doi:10.1172/jci42843 · Cited by 1,418 · see citing works
Davies, G., Lam, M., Harris, S. E., Trampush, J. W., Luciano, M., Hill, W. D., Hagenaars, S. P., Ritchie, S. J., Marioni, R. E., Fawns‐Ritchie, C., et al. (2018) · Nature Communications · doi:10.1038/s41467-018-04362-x · Cited by 668 · see citing works
Wallerian degeneration: an emerging axon death pathway linking injury and disease
Conforti, L., Gilley, J., & Coleman, M. P. (2014) · Nature reviews. Neuroscience · doi:10.1038/nrn3680 · Cited by 611 · see citing works
Self-citationEndogenous Nmnat2 Is an Essential Survival Factor for Maintenance of Healthy Axons
Gilley, J., & Coleman, M. P. (2010) · PLoS Biology · doi:10.1371/journal.pbio.1000300 · Cited by 472 · see citing works
Self-citationPeripheral thermosensation in mammals
Vriens, J., Nilius, B., & Voets, T. (2014) · Nature reviews. Neuroscience · doi:10.1038/nrn3784 · Cited by 453 · see citing works
Receptive Properties of Mouse Sensory Neurons Innervating Hairy Skin
Koltzenburg, M., Stucky, C. L., & Lewin, G. R. (1997) · Journal of Neurophysiology · doi:10.1152/jn.1997.78.4.1841 · Cited by 384 · see citing works
Sarm1-Mediated Axon Degeneration Requires Both SAM and TIR Interactions
Gerdts, J., Summers, D. W., Sasaki, Y., DiAntonio, A., & Milbrandt, J. (2013) · Journal of Neuroscience · doi:10.1523/jneurosci.1197-13.2013 · Cited by 359 · see citing works
Rigaud, M., Gemes, G., Barabas, M. E., Chernoff, D. I., Abram, S. E., Stucky, C. L., & Hogan, Q. H. (2008) · Pain · doi:10.1016/j.pain.2008.01.016 · Cited by 304 · see citing works
Prevention of vincristine-induced peripheral neuropathy by genetic deletion of SARM1 in mice
Geisler, S., Doan, R. A., Strickland, A. M., Huang, X., Milbrandt, J., & DiAntonio, A. (2016) · Brain · doi:10.1093/brain/aww251 · Cited by 272 · see citing works
Response Properties of Mechanoreceptors and Nociceptors in Mouse Glabrous Skin: An In Vivo Study
Cain, D. M., Khasabov, S. G., & Simone, D. A. (2001) · Journal of Neurophysiology · doi:10.1152/jn.2001.85.4.1561 · Cited by 264 · see citing works
Sasaki, Y., Vohra, B. P. S., Lund, F. E., & Milbrandt, J. (2009) · Journal of Neuroscience · doi:10.1523/jneurosci.5469-08.2009 · Cited by 243 · see citing works
Bartha, I., di Iulio, J., Venter, J. C., & Telenti, A. (2017) · Nature Reviews Genetics · doi:10.1038/nrg.2017.75 · Cited by 233 · see citing works
LaPointe, N. E., Morfini, G. A., Brady, S. T., Feinstein, S. C., Wilson, L., & Jordan, M. A. (2013) · NeuroToxicology · doi:10.1016/j.neuro.2013.05.008 · Cited by 219 · see citing works
Absence of SARM1 Rescues Development and Survival of NMNAT2-Deficient Axons
Gilley, J., Orsomando, G., Nascimento-Ferreira, I., & Coleman, M. (2015) · Cell Reports · doi:10.1016/j.celrep.2015.02.060 · Cited by 196 · see citing works
Self-citationNMNAT2:HSP90 Complex Mediates Proteostasis in Proteinopathies
Ali, Y., Allen, H. M., Yu, L., Li‐Kroeger, D., Bakhshizadehmahmoudi, D., Hatcher, A., Aubin, C., Xu, J., Bjorklund, N. L., Taglialatela, G., et al. (2016) · PLoS Biology · doi:10.1371/journal.pbio.1002472 · Cited by 128 · see citing works
Milde, S., Gilley, J., & Coleman, M. P. (2013) · PLoS Biology · doi:10.1371/journal.pbio.1001539 · Cited by 124 · see citing works
Self-citationRescue of Peripheral and CNS Axon Defects in Mice Lacking NMNAT2
Gilley, J., Adalbert, R., Yu, G., & Coleman, M. P. (2013) · Journal of Neuroscience · doi:10.1523/jneurosci.1534-13.2013 · Cited by 123 · see citing works
Self-citationSarm1 Deletion, but Not Wld, Confers Lifelong Rescue in a Mouse Model of Severe Axonopathy
Gilley, J., Ribchester, R. R., & Coleman, M. P. (2017) · Cell Reports · doi:10.1016/j.celrep.2017.09.027 · Cited by 121 · see citing works
Self-citationWldS protein requires Nmnat activity and a short N-terminal sequence to protect axons in mice
Conforti, L., Wilbrey, A. L., Morreale, G., Janečková, L., Beirowski, B., Adalbert, R., Mazzola, F., Stefano, M. D., Hartley, R., Babetto, E., et al. (2009) · The Journal of Cell Biology · doi:10.1083/jcb.200807175 · Cited by 113 · see citing works
Self-citationLjungberg, M. C., Ali, Y. O., Zhu, J., Wu, C.-S., Oka, K., Zhai, R. G., & Lu, H.-C. (2012) · Human Molecular Genetics · doi:10.1093/hmg/ddr492 · Cited by 107 · see citing works
Milde, S., Adalbert, R., Elaman, M. H., & Coleman, M. P. (2014) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2014.09.018 · Cited by 102 · see citing works
Self-citationStefano, M. D., Loreto, A., Orsomando, G., Mori, V., Zamporlini, F., Hulse, R. P., Webster, J., Donaldson, L. F., Gering, M., Raffaelli, N., et al. (2017) · Current Biology · doi:10.1016/j.cub.2017.01.070 · Cited by 95 · see citing works
Self-citationNMNATs, evolutionarily conserved neuronal maintenance factors
Ali, Y. O., Li-Kroeger, D., Bellen, H. J., Zhai, R. G., & Lu, H.-C. (2013) · Trends in Neurosciences · doi:10.1016/j.tins.2013.07.002 · Cited by 91 · see citing works
Hicks, A. N., Lorenzetti, D., Gilley, J., Lu, B., Andersson, K., Milligan, C., Overbeek, P. A., Oppenheim, R. W., & Bishop, C. E. (2012) · PLoS ONE · doi:10.1371/journal.pone.0047869 · Cited by 85 · see citing works
Self-citationMayer, P. R., Huang, N., Dewey, C. M., Dries, D. R., Zhang, H., & Yu, G. (2010) · Journal of Biological Chemistry · doi:10.1074/jbc.m110.178913 · Cited by 82 · see citing works
Self-citationHikosaka, K., Ikutani, M., Shito, M., Kazuma, K., Gulshan, M., Nagai, Y., Takatsu, K., Konno, K., Tobe, K., Kanno, H., et al. (2014) · Journal of Biological Chemistry · doi:10.1074/jbc.m114.554378 · Cited by 81 · see citing works
The gene for slow Wallerian degeneration (Wld(s)) is also protective against vincristine neuropathy.
Wang, M.-S., Wu, Y., Culver, D. G., & Glass, J. (2001) · Neurobiology of Disease · doi:10.1006/nbdi.2000.0334 · Cited by 77 · see citing works
Conforti, L., Janečková, L., Wagner, D. A., Mazzola, F., Cialabrini, L., Stefano, M. D., Orsomando, G., Magni, G., Bendotti, C., Smyth, N. R., et al. (2011) · FEBS Journal · doi:10.1111/j.1742-4658.2011.08193.x · Cited by 75 · see citing works
Self-citationAnalysis of protein-coding genetic variation in 60,706 humans
Atzmon, Palotie, A. V., Ripke, S., Rivas, M. A., Won, H., Freimer, Lyon, Rodríguez-Guillén, Barr, Weisburd, B., et al. (2020) · Carolina Digital Repository (University of North Carolina at Chapel Hill) · doi:10.17615/akst-av84 · Cited by 66 · see citing works
Slivicki, R. A., Ali, Y., Lu, H., & Hohmann, A. G. (2016) · PLoS ONE · doi:10.1371/journal.pone.0147620 · Cited by 21 · see citing works
Abram, S. E. (2009) · Yearbook of Anesthesiology and Pain Management · doi:10.1016/s1073-5437(08)79144-7 · Cited by 10 · see citing works
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NAD+ in Brain Aging and Neurodegenerative Disorders
Lautrup, S., Sinclair, D. A., Mattson, M. P., & Fang, E. F. (2019) · Cell Metabolism · doi:10.1016/j.cmet.2019.09.001 · Cited by 790 · see citing works
Programmed axon degeneration: from mouse to mechanism to medicine
Coleman, M. P., & Höke, A. (2020) · Nature reviews. Neuroscience · doi:10.1038/s41583-020-0269-3 · Cited by 320 · see citing works
Self-citationFigley, M. D., & DiAntonio, A. (2020) · Current Opinion in Neurobiology · doi:10.1016/j.conb.2020.02.012 · Cited by 145 · see citing works
Loreto, A., Hill, C. S., Hewitt, V. L., Orsomando, G., Angeletti, C., Gilley, J., Lucci, C., Sanchez-Martinez, A., Whitworth, A. J., Conforti, L., et al. (2020) · Neurobiology of Disease · doi:10.1016/j.nbd.2019.104678 · Cited by 131 · see citing works
Self-citationChemotherapy-Induced Peripheral Neuropathy: Mechanisms and Therapeutic Avenues
Bae, E. H., Greenwald, M. K., & Schwartz, A. G. (2021) · Neurotherapeutics · doi:10.1007/s13311-021-01142-2 · Cited by 125 · see citing works
Constitutively active SARM1 variants that induce neuropathy are enriched in ALS patients
Bloom, A. J., Mao, X. R., Strickland, A. M., Sasaki, Y., Milbrandt, J., & DiAntonio, A. (2022) · Molecular Neurodegeneration · doi:10.1186/s13024-021-00511-x · Cited by 118 · see citing works
Neuroprotection in glaucoma: Mechanisms beyond intraocular pressure lowering
Tribble, J. R., Hui, F., Quintero, H., Hajji, S. E., Bell, K. C., Polo, A. D., & Williams, P. A. (2023) · Molecular Aspects of Medicine · doi:10.1016/j.mam.2023.101193 · Cited by 115 · see citing works
Marion, C. M., McDaniel, D. P., & Armstrong, R. C. (2019) · Experimental Neurology · doi:10.1016/j.expneurol.2019.113040 · Cited by 81 · see citing works
Gilley, J., Jackson, O., Pipis, M., Estiar, M. A., Al‐Chalabi, A., Danzi, M. C., van Eijk, K. R., Goutman, S. A., Harms, M. B., Houlden, H., et al. (2021) · eLife · doi:10.7554/elife.70905 · Cited by 84 · see citing works
Self-citationStructural basis for RING-Cys-Relay E3 ligase activity and its role in axon integrity
Mabbitt, P. D., Loreto, A., Déry, M.-A. C., Fletcher, A. J., Stanley, M., Pao, K., Wood, N. T., Coleman, M. P., & Virdee, S. (2020) · Nature Chemical Biology · doi:10.1038/s41589-020-0598-6 · Cited by 78 · see citing works
Self-citationSelective inhibitors of SARM1 targeting an allosteric cysteine in the autoregulatory ARM domain
Feldman, H. C., Merlini, E., Guijas, C., DeMeester, K. E., Njomen, E., Kozina, E. M., Yokoyama, M., Vinogradova, E. V., Reardon, H. T., Melillo, B. N., et al. (2022) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.2208457119 · Cited by 79 · see citing works
Harlan, B. A., Killoy, K. M., Pehar, M., Liu, L., Auwerx, J. H., & Vargas, M. R. (2020) · Experimental Neurology · doi:10.1016/j.expneurol.2020.113219 · Cited by 70 · see citing works
Homozygous NMNAT2 mutation in sisters with polyneuropathy and erythromelalgia
Huppke, P., Wegener, E., Gilley, J., Angeletti, C. A., Kurth, I., Drenth, J. P. H., Stadelmann, C., Barrantes‐Freer, A., Brück, W., Thiele, H., et al. (2019) · Experimental Neurology · doi:10.1016/j.expneurol.2019.112958 · Cited by 67 · see citing works
Self-citationArthur‐Farraj, P., & Coleman, M. P. (2021) · Neurotherapeutics · doi:10.1007/s13311-021-01125-3 · Cited by 62 · see citing works
Self-citationImplications of NAD metabolism in pathophysiology and therapeutics for neurodegenerative diseases
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Mitochondrial dysfunction as a trigger of programmed axon death
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Self-citationTargeting Diet and Exercise for Neuroprotection and Neurorecovery in Glaucoma
Tribble, J. R., Hui, F., Jöe, M., Bell, K. C., Chrysostomou, V., Crowston, J. G., & Williams, P. A. (2021) · Cells · doi:10.3390/cells10020295 · Cited by 55 · see citing works
NMNAT2 is a druggable target to drive neuronal NAD production
Tribble, J. R., Jöe, M., Varricchio, C., Otmani, A., Canovai, A., Habchi, B., Daskalakis, E., Chaleckis, R., Loreto, A., Gilley, J., et al. (2024) · Nature Communications · doi:10.1038/s41467-024-50354-5 · Cited by 43 · see citing works
Self-citationMacrophage depletion blocks congenital SARM1-dependent neuropathy
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Cimaglia, G., Votruba, M., Morgan, J. E., André, H., & Williams, P. A. (2020) · Nutrients · doi:10.3390/nu12092871 · Cited by 39 · see citing works
Mechanisms of injury-induced axon degeneration
Ding, C., & Hammarlund, M. (2019) · Current Opinion in Neurobiology · doi:10.1016/j.conb.2019.03.006 · Cited by 36 · see citing works
Gould, S. A., Gilley, J., Ling, K., Jafar‐Nejad, P., Rigo, F., & Coleman, M. P. (2021) · Cell Reports · doi:10.1016/j.celrep.2021.110108 · Cited by 36 · see citing works
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“Thus, loss of the main axonal NMNAT isoform, NMNAT2, a protein absolutely required for axon survival [63, 64] appears to be what provides the axonal specificity of degeneration after axon injury, or in axonal transport disorders [65, 66], or when NMNAT2 is genetically disrupted [64, 67, 68, 69], since NMNAT1 supplies…”
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Lundt, S., & Ding, S. (2021) · Genes · doi:10.3390/genes12111776 · Cited by 27 · see citing works
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Self-citationPetropavlovskiy, A. A., Kogut, J. A., Leekha, A., Townsend, C. A., & Sanders, S. S. (2021) · Neuronal Signaling · doi:10.1042/ns20210005 · Cited by 23 · see citing works
Pathobiochemistry of Aging and Neurodegeneration: Deregulation of NAD+ Metabolism in Brain Cells
Kolotyeva, N. A., Groshkov, A. A., Rozanova, N. A., Berdnikov, A. K., Novikova, S. V., Komleva, Y. K., Salmina, A. B., Illarioshkin, S. N., & Пирадов, М. А. (2024) · Biomolecules · doi:10.3390/biom14121556 · Cited by 22 · see citing works
NMNAT2: An important metabolic enzyme affecting the disease progression
Li, W., Gao, M., Hu, C., Chen, X., & Zhou, Y. (2022) · Biomedicine & Pharmacotherapy · doi:10.1016/j.biopha.2022.114143 · Cited by 21 · see citing works
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Alexandris, A. S., & Koliatsos, V. E. (2023) · Antioxidants and Redox Signaling · doi:10.1089/ars.2023.0350 · Cited by 20 · see citing works
An adult-stage transcriptional program for survival of serotonergic connectivity
Kitt, M. M., Tabuchi, N., Spencer, W. C., Robinson, H. L., Zhang, X. L., Eastman, B., Lobur, K. J., Silver, J., Mei, L., & Deneris, E. S. (2022) · Cell Reports · doi:10.1016/j.celrep.2022.110711 · Cited by 19 · see citing works
Nmnat2 attenuates amyloidogenesis and up-regulates ADAM10 in AMPK activity-dependent manner
Cheng, X., Shi, F.-X., Zhao, K.-P., Lin, W., Li, X.-Y., Zhang, J., Bu, Y.-Y., Zhu, R., Li, X.-H., Duan, D.-X., et al. (2021) · Aging · doi:10.18632/aging.203634 · Cited by 18 · see citing works
Chiang, J. C. B., Arnold, R., Dhanapalaratnam, R., Markoulli, M. P., & Krishnan, A. V. (2022) · Pharmaceuticals · doi:10.3390/ph15050607 · Cited by 16 · see citing works
Zhu, Y., Lobato, A. G., Zhai, R. G., & Pinto, M. (2022) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2022.852972 · Cited by 14 · see citing works
Cartelli, D., Cavaletti, G., Lauria, G., & Meregalli, C. (2022) · Cells · doi:10.3390/cells11081358 · Cited by 13 · see citing works
Tang, B. L. (2019) · Cells · doi:10.3390/cells8030267 · Cited by 13 · see citing works
Programmed axon death: a promising target for treating retinal and optic nerve disorders
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Self-citationAdemi, M., Yang, X., Coleman, M. P., & Gilley, J. (2022) · Scientific Reports · doi:10.1038/s41598-022-18052-8 · Cited by 11 · see citing works
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Programmed axon degeneration: mechanism, inhibition and therapeutic potential
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Antoniou, C., Loreto, A., Gilley, J., Merlini, E., Orsomando, G., & Coleman, M. P. (2024) · Molecular Neurobiology · doi:10.1007/s12035-024-04480-2 · Cited by 8 · see citing works
Self-citationLiu, P., Huang, H., Fang, F., Liu, L., Li, L., Feng, X., Chen, W., Dalal, R., Sun, Y., & Hu, Y. (2021) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2021.754651 · Cited by 7 · see citing works
Guo, Y., Mehrabian, Z., Milbrandt, J., DiAntonio, A., & Bernstein, S. L. (2024) · Cells · doi:10.3390/cells13030202 · Cited by 6 · see citing works
Dingwall, C. B., Sasaki, Y., Strickland, A. M., Wu, T., Summers, D. W., Bloom, A. J., DiAntonio, A., & Milbrandt, J. (2025) · iScience · doi:10.1016/j.isci.2025.112626 · Cited by 6 · see citing works
Epplen, A. S. C., Rothöft, M., Stahlke, S., Theiß, C., & Matschke, V. (2025) · Cell Communication and Signaling · doi:10.1186/s12964-025-02415-5 · Cited by 5 · see citing works
Fat traffic control: S-acylation in axonal transport
Doerksen, A. H., Herath, N. N., & Sanders, S. S. (2025) · Molecular Pharmacology · doi:10.1016/j.molpha.2025.100039 · Cited by 5 · see citing works
SCFFBXO21-mediated ubiquitination and degradation of NMNAT2 regulates axon survival in nerve injury
Long, W., Li, S., Wang, Q., Yue, W., Fu, Y., Wang, H., Jiang, M., Hu, X., Li, Y., Cui, J., et al. (2025) · The Journal of Cell Biology · doi:10.1083/jcb.202501072 · Cited by 4 · see citing works
Base exchange inhibitors of SARM1 form mononucleotide adducts and activate SARM1 in vivoPreprint
Reardon, H. T., Guijas, C., Clapper, J. R., Callender, J. A., Kozina, E. M., Sarabia, F. J., Hutton, C., Herbst, D. M., Andalis, T., Perehinets, L., et al. (2025) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2025.04.22.649875 · Cited by 4 · see citing works
Transcriptional regulation of human NMNAT2 : insights from 3D genome sequencing and bioinformatics
Chang, Y. C., Yang, S., Cho, M., Nho, K. T., Baizabal, J., & Lu, H. (2025) · FEBS Journal · doi:10.1111/febs.70322 · Cited by 3 · see citing works
Gould, S. A., Gilley, J., Ling, K., Jaffar-Nejad, P., Ringo, F., & Coleman, M. P. (2021) · SSRN Electronic Journal · doi:10.2139/ssrn.3806068 · Cited by 2 · see citing works
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Hopkins, E. L., & Williams, P. A. (2026) · Experimental Neurology · doi:10.1016/j.expneurol.2026.115891 · Cited by 1 · see citing works
Yu, H., Feng, N., Zhong, W., Han, Y., Cheng, Y., Zhang, Z., Wang, Y., Gao, P., Huang, R., Zhang, C., et al. (2025) · The FASEB Journal · doi:10.1096/fj.202402546r · Cited by 1 · see citing works
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Coleman, M. P. (2020) · Methods in molecular biology · doi:10.1007/978-1-0716-0585-1_1 · Cited by 1 · see citing works
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Avetisyan, A. A., Manzo, E., Barria, R., Kocia, M., Hsu, J.-M., Larson, A., Weirnick, R., Balasubramanian, K., Blackwell, N., Freeman, M., et al. (2025) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2025.09.25.678663
Bloom, A. J., Mao, X., Strickland, A. M., Sasaki, Y., Milbrandt, J., & DiAntonio, A. (2022) · Figshare · doi:10.6084/m9.figshare.17982739
Bloom, A. J., Mao, X., Strickland, A. M., Sasaki, Y., Milbrandt, J., & DiAntonio, A. (2022) · Figshare · doi:10.6084/m9.figshare.17982727
Bloom, A. J., Mao, X., Strickland, A. M., Sasaki, Y., Milbrandt, J., & DiAntonio, A. (2022) · Figshare · doi:10.6084/m9.figshare.17982736
Bloom, A. J., Mao, X., Strickland, A. M., Sasaki, Y., Milbrandt, J., & DiAntonio, A. (2022) · Figshare · doi:10.6084/m9.figshare.17982742
Bloom, A. J., Mao, X., Strickland, A. M., Sasaki, Y., Milbrandt, J., & DiAntonio, A. (2022) · Figshare · doi:10.6084/m9.figshare.17982721
Bloom, A. J., Mao, X., Strickland, A. M., Sasaki, Y., Milbrandt, J., & DiAntonio, A. (2022) · Figshare · doi:10.6084/m9.figshare.17982733
Bloom, A. J., Mao, X., Strickland, A. M., Sasaki, Y., Milbrandt, J., & DiAntonio, A. (2022) · Figshare · doi:10.6084/m9.figshare.17982730
NAD+ signaling in Parkinson's disease: molecular mechanisms and therapeutic perspectives
Wang, T., Zhou, X., & Chen, X. (2026) · Frontiers in Neurology · doi:10.3389/fneur.2026.1943801
- Authors
- Gilley, J., Mayer, P. R., Yu, G., & Coleman, M. P.
- Affiliations
- Babraham Institute (GB)
- The University of Texas Southwestern Medical Center (US)
- Corresponding author
- Gilley, Jonathan
- Venue
- Human Molecular Genetics
- Publisher
- Oxford University Press (OUP)
- Published
- 2018-10-09
- Volume
- 28
- Issue
- 3
- Pages
- 448-458
- ISSN
- 0964-6906 (ISSN-L)
- 1460-2083
- OpenAlex
- W2897422184
- Cited by
- 62
- References
- 48
- Citations by year
- 2026: 2 · 2025: 9 · 2024: 6 · 2023: 4 · 2022: 17 · 2021: 11 · 2020: 6 · 2019: 7
- FWCI
- 2.73
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- academic.oup.com/journals/pages/open_access/funder_policies/chorus/standard_publication_model (vor)
- Locations
- Human Molecular Genetics (publishedVersion)
- PubMed (publishedVersion)
- Apollo (University of Cambridge) (submittedVersion)
- Apollo
- Funders
- Biotechnology and Biological Sciences Research Council
- Medical Research Council (MR/N004582/1)
- Ruth K. Broad Biomedical Research Foundation
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nerve injury and regeneration
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Hereditary Neurological Disorders
- Health Sciences › Medicine › Oncology › Cancer Treatment and Pharmacology
- Keywords
- NMNAT2, axon development, axon survival, compound heterozygosity, peripheral nerves, motor axons, temperature insensitivity, motor performance decline, neurite outgrowth, superior cervical ganglion neurons
- MeSH terms
- Age Factors, Animals, Axons, Female, Male, Nerve Degeneration, Neurons, Nicotinamide-Nucleotide Adenylyltransferase, Mice, Neurogenesis, Primary Cell Culture
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