About this Research Topic
Myelin, produced by oligodendrocytes (OLs) in the CNS and Schwann cells (SCs) in the PNS, gives the vertebrate nervous system with a functional advantage. This lipid-rich membrane provides trophic support and ensures the rapid and efficient propagation of action potentials. This increase in conduction velocity was fundamental for the emergence of complex behaviors during evolution.
Myelin is formed by the postnatal maturation of progenitor cells born during development. Our understanding of these events or mechanisms has been enriched by recently identified regulatory factors that control different aspects of their development and by large scale analysis showing a great diversity and complexity of progenitors and mature cells which could lead to distinct myelin structures. In addition, recent studies demonstrated a link between experiences and the generation of new myelin sheath or existing myelin remodeling. Even after the maturation phase, myelin could be shaped by environmental stimuli and undergo significant structural changes throughout life. This fine-tuning mechanism enhances neuronal function by adjusting in myelin structure, axo-glial interaction. The potential link between this adaptive myelination and neuropsychiatric conditions is an active area of research.
Alterations of the myelin structure or composition has been associated with the severity of different diseases. Following trauma, inflammatory and neurodegenerative pathologies such as Multiple Sclerosis (MS) or peripheral neuropathies, myelin can be damaged and this loss affects vital neurological functions. The extent of demyelination and associated axonal degeneration correlates with the degree of neurological decline. The available treatments can only ameliorate or prevent specific aspects of MS, while they fail to promote myelin restoration. Moreover, inherited demyelinating disorders of the CNS (Leukodystrophies) or the PNS (Charcot-Marie-Tooth-CMT neuropathies) remain incurable in most cases.
Although insufficient to allow complete functional recovery, a regenerative process can be observed. This self-repair potential represents great therapeutic hopes. Myelin repair can occur either as a result of changes in the structure of myelinated axons as well as in de novo myelination of other axons that have been either previously unmyelinated or damaged. New myelin formation occurs via recruitment and maturation of oligodendrocyte precursor cells (OPC) that persist in the adult CNS.
However, in an inflammatory environment, for example in MS brain, OPC often fail to remyelinate. Understanding the mechanisms behind this regenerative process would become crucial in identifying new therapeutic strategies. A lot has been learned about the biology of SCs through the discovery of over 100 genetic causes of inherited neuropathies, many of which result from mutations in SC-specific genes associated with demyelinating pathology. Likewise, autoimmune demyelinating neuropathies have revealed important molecular interactions controlling peripheral myelin integrity. Insights from human diseases and experimental models provide the basis for the development of new therapeutic approaches to treat peripheral demyelinating neuropathies.
This Research Topic aims to provide an overview and new perspectives on the myelin formation/repair mechanisms and novel therapeutic strategies that will lead to the development of new treatment for de-/dys-myelinating pathologies. This will help to prevent severe disabilities that have a serious impact on a patient’s everyday life as well as on society.
Keywords: Myelin, Oligodendrocytes, Schwann cells, Multiple Sclerosis, Peripheral Neuropathies
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