Molecular Insights into Myelin Dynamics: From Demyelination to Remyelination in Central Nervous System Diseases

Dear Colleagues,

The majority of vertebrate axons are encased in myelin, a lipid-dense sheath that significantly enhances neuronal signal transmission speed and efficiency. Additionally, the myelin sheath plays a role in supporting the axon by supplying essential nutrients, a mechanism referred to as metabolic coupling. In the central nervous system, oligodendrocytes—the glial cells responsible for forming myelin—can transfer energy substrates to axons through exosomes. If the metabolic and trophic support provided by oligodendrocytes is disrupted, it may lead to axonal degeneration and contribute to neurodegenerative processes. In contrast to what was believed till recently, myelin is a process that persists into late adulthood, suggesting that prolonged myelination might facilitate the precise adjustment of circuits during the life span of an individual. In addition to intrinsic mechanisms, there is also an adaptive myelination where myelin plasticity as a result of neuronal activity may modulate existing myelin sheaths or result in new ones. Demyelination, the damage of myelin, is evident in multiple sclerosis as well as other neurodegenerative diseases (AD, PD, etc.), while remyelination is a spontaneous attempt at repair. Ongoing efforts are directed towards identifying substances that promote remyelination.

We invite the myelin research community to contribute both original research articles and reviews covering studies on myelination and remyelination. Both basic and translational research papers are welcome.

Prof. Dr. Domna Karagogeos
Guest Editor

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