We initially hypothesized that injured axons fail to present Contactin, a positive ligand for the oligodendroglial Notch1 receptor to induce myelination, and thus tracked axoglial Contactin/Notch1 signaling in situ, using immunohistochemistry in brain tissue from MS patients containing chronic demyelinated lesions.
In this issue of the JCI, Nakahara et al. show that Contactin is abundantly expressed on demyelinated axons in human chronic MS lesions and that Notch1 is activated in oligodendrocyte precursor cells (see the related article beginning on page 169).