Myelination and the trophic support of long axons
Open accessAbstract
In addition to their role in providing myelin for rapid impulse propagation, the glia that ensheath long axons are required for the maintenance of normal axon transport and long-term survival. This presumably ancestral function seems to be independent of myelin membrane wrapping. Here, I propose that ensheathing glia provide trophic support to axons that are metabolically isolated, and that myelin itself might cause such isolation. This glial support of axonal integrity may be relevant for a number of neurological and psychiatric diseases.
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Failure of OLs' energy-trophic function may contribute to axonal neurodegeneration.
“Failure of OLs’ energy-trophic function may contribute to such axonal neurodegeneration [302,303].”
From Revisiting the Pathogenesis of X-Linked Adrenoleukodystrophy (2025) · cites this paper as [302]
Axons require oligodendroglial support mostly after myelination, which limits rapid axonal access to extracellular metabolites.
“suggesting that axons require oligodendroglial support mostly after myelination, which limits rapid axonal access to extracellular metabolites”
From Oligodendroglial NMDA receptors regulate glucose import and axonal energy metabolism (2016) · cites this paper as Nave, 2010
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Subtle myelin defects in PLP‐null mice
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How neuroinflammation contributes to neurodegeneration
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The Pathobiology of Vascular Dementia
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“Importantly, axonal recovery after OGD was normal prior to age P10 (Figure S6A), suggesting that axons require oligodendroglial support mostly after myelination, which limits rapid axonal access to extracellular metabolites (Nave, 2010).”
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“A vital aspect of this protection is believed to stem from the nutritional support glial cells provide to axons [89,90].”
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- Authors
- Nave, K.-A.
- Affiliations
- Max Planck Institute of Experimental Medicine (DE)
- Corresponding author
- Nave, Klaus-Armin
- ORCID
- Nave, Klaus-Armin
- Venue
- Nature Reviews Neuroscience
- Published
- 2010-03-10
- Volume
- 11
- Issue
- 4
- Pages
- 275-283
- ISSN
- 1471-003X (ISSN-L)
- 1471-0048
- OpenAlex
- W1980230515
- Cited by
- 648
- References
- 141
- Citations by year
- 2026: 20 · 2025: 39 · 2024: 34 · 2023: 44 · 2022: 46 · 2021: 46 · 2020: 45 · 2019: 41 · 2018: 44 · 2017: 37 · 2016: 40 · 2015: 50 · 2014: 48 · 2013: 46 · 2012: 29
- FWCI
- 3.25
- Type
- journal article
- Language
- en
- Open access
- green
- zenodo.org
- Licence
- other-oa
- www.springer.com/tdm (tdm)
- Locations
- Nature reviews. Neuroscience (publishedVersion)
- PubMed (publishedVersion)
- MPG.PuRe (Max Planck Society) (submittedVersion)
- Zenodo (CERN European Organization for Nuclear Research) (submittedVersion, other-oa)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nerve injury and regeneration
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Keywords
- myelination, ensheathing glia, axon survival, axonal transport, myelin, axon integrity, neurological disorders, mental illness
- MeSH terms
- Animals, Axons, Axonal Transport, Demyelinating Diseases, Humans, Models, Neurological, Myelin Sheath, Nerve Degeneration, Neuroglia
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