This issue first comprehensively overviewed the molecular regulation of oligodendrocyte specification and timing control of differentiation, as well as the active participation of NG2-positive polydendrocyte, a special type of oligodendrocyte progenitor, in myelin repair following demyelinating lesions. Then the formation of compact myelin sheaths around axons, which accompanies the oligodendrocyte differentiation, is reviewed. Some interesting topics include negative regulation of axonal myelination, and the control of numbers and lengths of myelin internodes formed by oligodendrocytes. Once myelin is formed, this issue further goes into the extensive and intimate interactions between axons and oligodendrocyte processes. As a demyelinating disease, multiple sclerosis has been extensively studied, with some emerging therapeutic concepts including promoting remyelination and adult NG2+ cell transplantation for its treatment. Also needs attention is the paticipation of microglia and macrophages in its pathogenesis. Last but not least, demyelination can be selectively induced in the corpus callosum by cuprizone, which can cause deficits in exploratory behavior. Interestingly, the vulnerability of myelin to this chemical appears to be age-dependent.

We hope that this collection of thorough and thoughtful papers will encourage further identification and characterization of regulatory molecules in normal myelination, and more importantly, developing novel molecular and cellular approaches to facilitating myelin repair in demyelinating diseases and in spinal cord/brain injury.