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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.
Brain region-specific oligodendrocyte population dynamics are unclear. Here the authors implement long-term in vivo three-photon imaging to determine those dynamics in the cortical and subcortical areas in the living intact and demyelinated adult mouse brain.
Oligodendrocytes are vulnerable to chemical toxicity during development. However, few environmental chemicals have been identified as potential hazards. Here, the authors discover chemicals in common household products as harmful to oligodendrocyte development.
Factors limiting CNS remyelination with age are poorly understood. Here the authors show that aged Treg lose capacity to support CNS remyelination in mice, which can be restored in a young environment.
Myelinated axons vary in diameter by over 100-fold. Here, the authors identify a role for the nuclear transport receptor importin 13 in axon diameter growth and corresponding increases to conduction speed along myelinated axons.
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.
