Matute C, et al. - Given that in patients with anti-NMDAR encephalitis, antibodies against neuronal N-methyl-D-aspartate receptors (NMDARs) modify neuronal synaptic function and plasticity, researchers here sought to determine the effects on other cells of the nervous system. In the studies, they used CSF of patients with anti-NMDAR encephalitis (preabsorbed or not with GluN1) and a human NMDAR specific monoclonal antibody (SSM5) derived from plasma cells of a patient, along with the corresponding controls. A functional assay based on cytosolic Ca2+ imaging was employed to estimate the activity of oligodendrocyte NMDARs and AMPARs in vitro after exposure to patients' CSF antibodies or SSM5. Immunocytochemistry was used to assess the expression of the glucose transporter (GLUT1) in oligodencrocytes. Outcomes suggest that antibodies from patients with anti-NMDAR encephalitis particularly modify the function of NMDAR in oligodendrocytes producing a reduction in expression of GLUT1. Considering the necessity of normal GLUT1 expression in oligodendrocytes and myelin to metabolically support axonal function, outcomes imply a connection between antibody-mediated dysfunction of NMDAR in oligodendrocytes and the white matter modifications inscribed in cases with this disorder.