BACKGROUND: Damage to astrocytes by anti-aquaporin-4 antibody (AQP4-Ab), also known as NMO antibody, has been implicated as the cause of neuromyelitis optica. Myelin oligodendrocyte glycoprotein (MOG) is well known as the causative protein of multiple sclerosis (MS). MOG antigen is currently considered as a cause of optic neuritis (ON) associated with MS because immunization with MOG antigen derived from oligodendrocytes induces murine ON with myelitis. We investigated the relationship between NMO antibody (NMO-Ab) and anti-MOG antibody (MOG-Ab) and potential in patients with ON for recovery of vision. METHODS: Thirty-three eyes of 23 patients with ON were studied. At presentation, serum NMO-Ab was measured by immunofluorescence using HEK 293 cells transfected with AQP4-GFP, and anti-MOG1-125 antibody was measured by enzyme-linked immunosorbent assay. MOG-Ab seropositivity was defined by comparing with MOG-Ab level obtained from 8 healthy normal subjects. RESULTS: Eleven (47%) of 23 ON patients were NMO-Ab seropositive, while 8 (34%) of the 23 patients were MOG-Ab seropositive. Six (26%) of 23 patients were seropositive for both NMO-Ab and MOG-Ab. Ten (43%) of 23 patients were seronegative for both antibodies. Three (50%) of 6 eyes of patients seropositive for both antibodies did not respond to corticosteroid pulse therapy and plasmapheresis, and visual acuity remained unchanged. In the NMO-Ab/MOG-Ab group, visual acuity improved significantly (P < 0.0001). In the other 3 groups (NMO-Ab/MOG-Ab, NMO-Ab/MOG-Ab, and NMO-Ab/MOG-Ab), visual acuity did not change significantly (P = 0.53, 0.42, and 0.45, respectively). CONCLUSION: NMO-Ab and MOG-Ab could be potential biomarkers to determine visual prognosis in patients with ON.
BACKGROUND: Damage to astrocytes by anti-aquaporin-4 antibody (AQP4-Ab), also known as NMO antibody, has been implicated as the cause of neuromyelitis optica. Myelin oligodendrocyte glycoprotein (MOG) is well known as the causative protein of multiple sclerosis (MS). MOG antigen is currently considered as a cause of optic neuritis (ON) associated with MS because immunization with MOG antigen derived from oligodendrocytes induces murine ON with myelitis. We investigated the relationship between NMO antibody (NMO-Ab) and anti-MOG antibody (MOG-Ab) and potential in patients with ON for recovery of vision. METHODS: Thirty-three eyes of 23 patients with ON were studied. At presentation, serum NMO-Ab was measured by immunofluorescence using HEK 293 cells transfected with AQP4-GFP, and anti-MOG1-125 antibody was measured by enzyme-linked immunosorbent assay. MOG-Ab seropositivity was defined by comparing with MOG-Ab level obtained from 8 healthy normal subjects. RESULTS: Eleven (47%) of 23 ON patients were NMO-Ab seropositive, while 8 (34%) of the 23 patients were MOG-Ab seropositive. Six (26%) of 23 patients were seropositive for both NMO-Ab and MOG-Ab. Ten (43%) of 23 patients were seronegative for both antibodies. Three (50%) of 6 eyes of patients seropositive for both antibodies did not respond to corticosteroid pulse therapy and plasmapheresis, and visual acuity remained unchanged. In the NMO-Ab/MOG-Ab group, visual acuity improved significantly (P < 0.0001). In the other 3 groups (NMO-Ab/MOG-Ab, NMO-Ab/MOG-Ab, and NMO-Ab/MOG-Ab), visual acuity did not change significantly (P = 0.53, 0.42, and 0.45, respectively). CONCLUSION:NMO-Ab and MOG-Ab could be potential biomarkers to determine visual prognosis in patients with ON.
Authors: Eric D Gaier; Katherine Boudreault; Joseph F Rizzo; Julie Falardeau; Dean M Cestari Journal: Curr Neurol Neurosci Rep Date: 2015-12 Impact factor: 5.081
Authors: Patrick Waters; Mark Woodhall; Kevin C O'Connor; Markus Reindl; Bethan Lang; Douglas K Sato; Maciej Juryńczyk; George Tackley; Joao Rocha; Toshiyuki Takahashi; Tatsuro Misu; Ichiro Nakashima; Jacqueline Palace; Kazuo Fujihara; M Isabel Leite; Angela Vincent Journal: Neurol Neuroimmunol Neuroinflamm Date: 2015-03-19