Höftberger R, Guo Y, Flanagan EP, et al. - Researchers histopathologically examined 2 autopsies and 22 brain biopsies from individuals with CNS inflammatory demyelinating diseases seropositive for myelin oligodendrocyte glycoprotein (MOG)-antibody by live-cell-based-assay with full-length MOG in its conformational form. Myelin oligodendrocyte glycoprotein antibody-associated disorders autopsies (ages 52 and 67) show the full spectrum of histopathological features observed within the 22 brain biopsies (median age, 10 years; range, 1–66; 56% female). Despite argues against endocytic internalization of the MOG antigen complement deposition in the absence of selective MOG protein loss suggest humoral mechanisms are involved. Parallels with MOG-EAE imply MOG may be an amplification factor that augments CNS demyelination, likely via complement-mediated destruction of myelin or antibody-dependent cellular cytotoxicity phagocytosis.