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Review: Treatment of neuromyelitis optica: Current debate
Tomoko Okamoto
Department of Neurology, Musashi Hospital, National Center of Neurology and Psychiatry, Kodaira, Tokyo, Japan
Masafumi Ogawa
Department of Neurology, Musashi Hospital, National Center of Neurology and Psychiatry, Kodaira, Tokyo, Japan
Youwei Lin
Department of Immunology, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Kodaira, Tokyo, Japan
Miho Murata
Department of Neurology, Musashi Hospital, National Center of Neurology and Psychiatry, Kodaira, Tokyo, Japan
Sachiko Miyake
Department of Immunology, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Kodaira, Tokyo, Japan
Takashi Yamamura
Department of Immunology, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Kodaira, Tokyo, Japan, yamamura{at}ncnp.go.jp
Neuromyelitis optica (NMO) is an inflammatory demyelinating disease that largely affects optic nerves and spinal cord. Recent studies have identified an elevation of serum anti-aquaporin 4 antibody as a hallmark of NMO. Typical cases of NMO significantly differ from multiple sclerosis (MS) in immunological markers, histopathology, and responses to therapy. In fact, plasma exchange may be more efficacious for NMO than MS, whereas interferon-β is recommended for MS but not for NMO. An emerging idea that pathogenesis of NMO may involve an interaction of the newly identified helper T cell subset, Th17, with B cells offers potential targets of therapy.
Key Words: neuromyelitis optica multiple sclerosis Th17 cells anti-aquaporin-4 antibody interferon-β
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Therapeutic Advances in Neurological Disorders, Vol. 1, No. 1,
43-52 (2008)
DOI: 10.1177/1756285608093978

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