Axonal degeneration is blocked by nicotinamide mononucleotide adenylyltransferase (NMNAT) protein transduction into transected axons
Open accessAbstract
Axonal degeneration is an early and important component of many neurological disorders. Overexpression of nicotinamide mononucleotide adenylyltransferase (Nmnat), a component of the slow Wallerian degeneration (Wld(s)) protein, protects axons from a variety of insults. We found that transduction of Nmnat protein into severed axons via virus-like particles prevented axonal degeneration. The post-injury efficacy of Nmnat indicates that its protective effects occur locally within the axon and provides an opportunity to develop novel agents to treat axonal damage.
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In mammals, over-expressing NMNATs significantly delays Wallerian degeneration of peripheral nerves.
“In mammals, over-expressing NMNATs significantly delays Wallerian degeneration of peripheral nerves (28)(29)(30)(31)(32)(33).”
From CREB-activity and nmnat2 transcription are down-regulated prior to neurodegeneration, while NMNAT2 over-expression is neuroprotective, in a mouse model of human tauopathy (2012) · cites this paper as [31]
The opening section says Nmnat1 overexpression can delay axonal degeneration, and Results and Discussion reports axonal protection in transgenic mice expressing Nmnat proteins. The paper’s own experiments use cultured dorsal-root-ganglion neurons; our copy does not establish the more specific claim that overexpression significantly delays Wallerian degeneration of peripheral nerves in vivo. (LLM, conf=0.84)
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Cites
Axon degeneration mechanisms: Commonality amid diversity
Coleman, M. (2005) · Nature reviews. Neuroscience · doi:10.1038/nrn1788 · Cited by 819 · see citing works
Yahata, N., Yuasa, S., & Araki, T. (2009) · The Journal of Neuroscience · doi:10.1523/jneurosci.4304-08.2009 · Cited by 154 · see citing works
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Research works printed but not linked: 1
- Miller, B. R., Press, C., Daniels, R. W., Sasaki, Y., Milbrandt, J., and Di- Antonio, A. (2009) Nat. Neurosci. 12, 387-389
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SARM1 activation triggers axon degeneration locally via NAD <sup>+</sup> destruction
Gerdts, J., Brace, E. J., Sasaki, Y., DiAntonio, A., & Milbrandt, J. (2015) · Science · doi:10.1126/science.1258366 · Cited by 593 · see citing works
Self-citationNMNAT1 inhibits axon degeneration via blockade of SARM1-mediated NAD+ depletion
Sasaki, Y., Nakagawa, T., Mao, X., DiAntonio, A., & Milbrandt, J. (2016) · eLife · doi:10.7554/elife.19749 · Cited by 192 · see citing works
Self-citationGoyal, M. S., Venkatesh, S., Milbrandt, J., Gordon, J. I., & Raichle, M. E. (2015) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1511465112 · Cited by 141 · 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
NMNATs, 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
- Authors
- Sasaki, Y., & Milbrandt, J.
- Affiliations
- Washington University in St. Louis (US)
- Corresponding author
- Milbrandt, Jeffrey
- ORCID
- Milbrandt, Jeffrey
- Venue
- Journal of Biological Chemistry
- Publisher
- Elsevier BV
- Published
- 2010-12
- Volume
- 285
- Issue
- 53
- Pages
- 41211-41215
- ISSN
- 0021-9258 (ISSN-L)
- PMC
- PMC3009846
- OpenAlex
- W2039624926
- Cited by
- 66
- References
- 2
- Citations by year
- 2026: 2 · 2025: 1 · 2024: 1 · 2023: 3 · 2022: 4 · 2021: 5 · 2020: 4 · 2019: 6 · 2018: 1 · 2017: 4 · 2016: 4 · 2015: 6 · 2014: 5 · 2013: 6 · 2012: 10
- FWCI
- 2.59
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Biological Chemistry (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Craig H. Neilsen Foundation
- Muscular Dystrophy Association
- Hope Center for Neurological Disorders (P30 NS057105)
- National Institutes of Health (AG13730, NS057105, NS065053)
- Health Science Center, University of Tennessee
- National Institute on Aging (AG 13730, R01AG013730)
- National Institute of Neurological Disorders and Stroke (R01NS065053, P30NS057105, NS065053, NS070053, R21NS070053)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nerve injury and regeneration
- Life Sciences › Neuroscience › Neurology › Neurological Disorders and Treatments
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Hereditary Neurological Disorders
- Keywords
- axonal degeneration, nicotinamide mononucleotide adenylyltransferase, Wallerian degeneration, virus-like particles, protein transduction, axon transection, axonal protection, axonal injury
- MeSH terms
- Animals, Axons, Cell Line, Cells, Cultured, Ganglia, Spinal, Humans, Models, Biological, Models, Neurological, Neurons, Nicotinamide-Nucleotide Adenylyltransferase, Proteins, Lentivirus, Neurodegenerative Diseases, Mice
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