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- W2026942912 abstract "Neuromyelitis optica (NMO) is a relapsing inflammatory disease that derives its name from its prominent affliction of optic nerves and spinal cord.1 Once regarded as a demyelinating variant of multiple sclerosis (MS), NMO is now causally associated with disease-specific autoantibodies (NMO–immunoglobulin G [IgG]) that bind selectively to aquaporin-4 (AQP4) water channels, which in the CNS are located exclusively on astrocytes.2 The presence of such autoantibodies raises questions regarding their precise roles in generating NMO symptoms and lesions. To date, the focus in NMO has been on severe symptoms such as vision loss and paralysis1 that are associated with prominent lesions in which complement-mediated astrocyte lysis may underlie or contribute to pronounced inflammation and tissue destruction.3,4In this issue of Neurology ®, Popescu et al.5 provide compelling evidence that circulating NMO-IgG (i.e., autoantibodies to AQP4) mediate symptoms of nausea and vomiting in NMO without causing astrocyte loss or tissue destruction. They report 3 main findings. First, about 40% of a cohort of neuropathologic specimens from patients with NMO exhibited anatomic changes in the area postrema, whereas such changes were not found in control specimens …" @default.
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- W2026942912 date "2011-03-02" @default.
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- W2026942912 title "Neuromyelitis optica: Circulating autoantibodies provoke astrocyte-mediated neural dysfunction" @default.
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- W2026942912 doi "https://doi.org/10.1212/wnl.0b013e3182143355" @default.
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