AQP4 is preserved, with absence of dystrophic astrocytes, and variable oligodendrocyte and axonal destruction. Complement deposition is present in all active white matter lesions, but a preferential loss of MOG is not observed. A CD4+ T-cell dominated inflammatory reaction with granulocytic infiltration predominates. Radially expanding confluent slowly expanding smoldering lesions in the white matter as seen in MS, are not present. MOGAD pathology is dominated by coexistence of both perivenous and confluent white matter demyelination, with an over-representation of intracortical demyelinated lesions compared to typical MS. Clinical, radiologic, and laboratory characteristics and course (78% relapsing) are consistent with MOGAD. MOGAD autopsies (ages 52 and 67) demonstrate the full spectrum of histopathological features observed within the 22 brain biopsies (median age, 10 years range, 1–66 56% female). We histopathologically analyzed 2 autopsies and 22 brain biopsies from patients with CNS inflammatory demyelinating diseases seropositive for MOG-antibody by live-cell-based-assay with full length MOG in its conformational form. We sought to define the pathological features of myelin oligodendrocyte glycoprotein (MOG) antibody associated disorders (MOGAD) in an archival autopsy/biopsy cohort.
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