The DOI matches its Crossref record; 122 of the 122 references it cites were found in a registry or an index.
Axon degeneration mechanisms: commonality amid diversity
Abstract
A wide range of insults can trigger axon degeneration, and axons respond with diverse morphology, topology and speed. However, recent genetic, immunochemical, morphological and pharmacological investigations point to convergent degeneration mechanisms. The principal convergence points - poor axonal transport, mitochondrial dysfunction and an increase in intra-axonal calcium - have been identified by rescuing axons with the slow Wallerian degeneration gene (Wld(S)) and studies with blockers of sodium or calcium influx. By understanding how the pathways fit together, we can combine our knowledge of mechanisms, and potentially also treatment strategies, from different axonal disorders.
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“Another important factor might be the disruption of fast axonal transport, resulting in focal swellings filled with various organelles, as seen in the vicinity but also distant from plaques in several AD transgenic models [27,28,29,30], resembling Wallerian degeneration [31].”
From Neuron Loss in Alzheimer’s Disease: Translation in Transgenic Mouse Models (2020) · cites this paper as [31]
In the citing paper
“The principal mechanisms of axon degeneration are metabolic stress, disturbed axonal transport, and mitochondrial dysfunction [301].”
From Revisiting the Pathogenesis of X-Linked Adrenoleukodystrophy (2025) · cites this paper as [301]
Citations
Cites
Alzheimer's Disease Is a Synaptic Failure
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Amyotrophic lateral sclerosis is a distal axonopathy: evidence in mice and man
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Axonopathy and Transport Deficits Early in the Pathogenesis of Alzheimer’s Disease
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Increased Nuclear NAD Biosynthesis and SIRT1 Activation Prevent Axonal Degeneration
Araki, T., Sasaki, Y., & Milbrandt, J. (2004) · Science · doi:10.1126/science.1098014 · Cited by 1,060
Disruption of Cnp1 uncouples oligodendroglial functions in axonal support and myelination
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Research works printed but not linked: 1
- Wishart, T. M. et al. Transcriptional regulation of pituitary tumour transforming gene-1 by the neuroprotective WldS gene in mouse cerebellar granule cells and HEK293 cell lines. J. Physiol. 565P, C74 (2004).
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Martínez, N. W., Manzano, C. M., Trujillo, A., Pizarro, I. S., Barrera, D. P., Calvo, M., & Matus, S. (2026) · Research Square · doi:10.21203/rs.3.rs-9204935/v1
Yap, Y., Musgrove, R. E., Breadmore, M. C., Guijt, R. M., Wilson, R., Wertheimer, G., King, A. E., & Dickson, T. C. (2026) · Microsystems & Nanoengineering · doi:10.1038/s41378-026-01187-3
Functional Pathological Features and Molecular Markers in Alzheimer’s Disease
Park, M.-N., Kim, H. W., Hong, J., Kim, J. K., Lee, S.-B., Baek, H. S., Kwak, S., Kwon, Y. J., Park, K., Jeon, J., et al. (2026) · International Journal of Molecular Sciences · doi:10.3390/ijms27114720
Pérez-Villavicencio, J., Villa-Robledo, O., Megchun-Vázquez, X., Uriarte-Jiménez, F., Rubio‐Osornio, M., & Serrano‐García, N. (2026) · Neuroglia · doi:10.3390/neuroglia7030023
Huang, C.-W., Chang, H.-I., Chang, T., Lin, K., Hsu, S., Lee, C.-C., Huang, S., & Chang, C. (2026) · European Journal of Nuclear Medicine and Molecular Imaging · doi:10.1007/s00259-026-08121-9
Ericson, M. O. (2026) · Frontiers in Neuroscience · doi:10.3389/fnins.2026.1940938
Slow-Wave Enhancement Reduces Axonal Injury in Murine Traumatic Brain Injury
Morawska, M. M., Moreira, C. G., Sahasrabudhe, D., Lane, L. T., Dias, I., Scammell, T. E., Noaín, D., & Baumann, C. R. (2026) · Neurotrauma Reports · doi:10.1177/2689288x261473740
Identification of a septin filament required for CNS myelin integrity
Patzig, J. (2014) · eDiss (Georg-August-Universität Göttingen) · doi:10.53846/goediss-4455
Saul, A. (2013) · eDiss (Georg-August-Universität Göttingen) · doi:10.53846/goediss-3915
Metadata
- Authors
- Coleman, M.
- Affiliations
- Babraham Institute (GB)
- Corresponding author
- Coleman, Michael
- ORCID
- Coleman, Michael
- Venue
- Nature reviews. Neuroscience
- Published
- 2005-10-14
- Volume
- 6
- Issue
- 11
- Pages
- 889-898
- ISSN
- 1471-003X (ISSN-L)
- 1471-0048
- OpenAlex
- W2042991032
- Cited by
- 819
- References
- 122
- Citations by year
- 2026: 15 · 2025: 30 · 2024: 13 · 2023: 22 · 2022: 18 · 2021: 35 · 2020: 40 · 2019: 32 · 2018: 40 · 2017: 48 · 2016: 43 · 2015: 51 · 2014: 47 · 2013: 58 · 2012: 53
- FWCI
- 2.91
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature reviews. Neuroscience (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Biotechnology and Biological Sciences Research Council
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nerve injury and regeneration
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Hereditary Neurological Disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Autophagy in Disease and Therapy
- Keywords
- axonal degeneration, Wallerian degeneration, axonal transport, mitochondrial dysfunction, intracellular calcium, sodium influx, calcium influx
- MeSH terms
- Animals, Axons, Axonal Transport, Central Nervous System, Humans, Nerve Tissue Proteins, Wallerian Degeneration
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