Myelination and the trophic support of long axons
By K. Nave. Nature Reviews Neuroscience, 2010
642 citations recorded by the source corpus.
Subfields: Cellular and Molecular Neuroscience, Developmental Neuroscience, Neurology
View Paper: https://www.semanticscholar.org/paper/a1d4617d20d531d6518a521c5f5c222c6fe00e4b
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In Cellular and Molecular Neuroscience
In Developmental Neuroscience
In Neurology
Citations in the corpus
- Neurotransmitter-Triggered Transfer of Exosomes Mediates Oligodendrocyte–Neuron Communication (2013, neutral): “function independent of myelination [7].”
- Myelination and support of axonal integrity by glia (2010, background): “Neurological diseases that are known to have a primary origin in the glia cause length-dependent axon loss (see 'Myelin diseases leading to axonal degeneration'), showing that long axons profit from the intimate interaction with local glial cell”
- NG2+ CNS glial progenitors remain committed to the oligodendrocyte lineage in postnatal life and following neurodegeneration. (2010, background): “Moreover, because OLs are crucial for metabolic support of axons (Nave, 2010), a loss of OLs may further accelerate neuronal degeneration.”
- Oligodendrocytes: Myelination and Axonal Support. (2015, background): “As a “myelinic channel,” this tube-like cytosolic compartment (also termed the “inner lip”) runs in parallel to the thin extracellular periaxonal space in which it faces the axonal in-ternode along its length (Nave 2010).”