Multiple sclerosis (MS) is the most frequent demyelinating disease affecting the adult central nervous system (CNS) with a broad range of symptoms (fatigue, depression, severe mobility etc…). Its cause is the loss of myelin, the lipid sheaths surrounding axons that enable the neural fast transmission. In the CNS, myelin is produced by oligodendrocytes (OLs), whose tasks are axonal insulation and trophic support1,2. Although the regeneration/recovery of myelin (remyelination) occurs efficiently in MS experimental models, remyelination is heterogeneous among MS patients, decreasing overtime. As a result, prolonged demyelination induces neurodegeneration and more severe and irreversible clinical outcomes. To highlight, clinical recovery of MS patients is associated with remyelination3, suggesting the potential benefit of promoting remyelination. To date, the majority of drugs developed for MS target the inflammatory pathways, helping to face MS relapses, but with no success in boosting myelin repair and preventing neurodegeneration.

There are no promising therapies for the progressive forms of MS, such as drugs promoting remyelination, which could slow down/stop neurodegeneration and therefore, patient disability. This reality highlights that enhancing remyelination is an obvious need to improve the clinical outcome of MS patients. A better knowledge in the remyelination field is essential to find novel and successful approaches to boost myelin repair and MS patient quality of life.