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Myelin biology and repair refers to the science of myelin physiology, manufacture, and how myelin damage in either the peripheral or central nervous systems can be repaired. Myelin – produced by Schwann cells in the periphery and oligodendrocytes in the CNS – is defective in diseases such as multiple sclerosis, and many myelin repair strategies aim to mitigate this damage.
Myelination is often compromised in ATR-X intellectual disability syndrome patients. Here, the authors show that the causative gene, ATRX, can regulate myelination in mice by modulating systemic thyroxine levels and by supporting oligodendrocyte progenitor differentiation.
Demyelination is often suggested to cause axonal degeneration. Here, the authors study mice carrying distinct PLP defects and reveal how persistent ensheathment with perturbed myelin poses a risk for CD8 + T cell-driven axon loss and behavioral decline.
How and to what extent oligodendrocytes (OLs) contribute to learning and cognition is not well understood. Here, the authors show that the performance of mice in working memory-dependent cognitive tasks depends on OL genesis and is proportional to the number of OL precursors and OLs generated during training.
By studying axonal pathology in human multiple sclerosis and its models, we observed that myelin ensheathment itself can be detrimental for axonal survival. We hypothesize that oligodendroglial support is disrupted under inflammatory conditions, with the most severe consequences for the axons that remain physically isolated from the extracellular milieu by myelin.
Learning requires new oligodendrogenesis, but how myelin patterns change during learning is unclear. Bacmeister et al. show that motor learning induces phase-specific changes in myelination on behaviorally activated axons that correlate with motor performance, suggesting myelin remodeling is involved in learning.
In rodents, absence seizures — a prominent manifestation of generalized epilepsy — drive activity-dependent myelination in the corpus callosum, increase interhemispheric synchrony and drive increases in seizure burden over time.
Activity-regulated myelination adaptively tunes neural circuit function in health. In rodent models of generalized epilepsy, recurrent seizures aberrantly increase myelination specifically within the seizure circuit. Blocking this seizure-induced myelination abrogates the progressive increase in seizure burden and ictal hypersynchrony that occurs in mice with intact activity-regulated myelination, indicating that maladaptive myelination can contribute to disease progression in epilepsy.
