Lesions in multiple sclerosis (MS) are characterized by inflammation, oligodendrocytes (OL) death and demyelination as well as axon lesions. The remyelination failure associates with persistent axonal alterations [1, 2], and this results in permanent disability for patients. These axon lesions can occur early in the course of the disease [3], but their origin is equivocal. They could result directly from inflammation, or they could be secondary to prolonged demyelination [4]. It is striking that experimentally remyelination alleviates them [5, 6]. [...