Early and extensive alterations of glial Cxs, particularly loss of membranous Cx32 in oligodendrocytic somata and myelin and Cx32 re‐distribution to the oligodendrocytic cytoplasm in MSA may accelerate distal oligodendrogliopathy type demyelination and nodal/paranodal dysfunction through disruption of inter‐glial communication. Here, GJB1 is linked to multiple system atrophy.