Astrocyte loss induced by neuromyelitis optica (NMO)-IgG and complement-dependent cytotoxicity (CDC) is the hallmark of NMO pathology. The survival of astrocytes is thought to reflect astrocyte exposure to environmental factors in the CNS and the response of astrocytes to these factors. However, still unclear are how astrocytes respond to NMO-IgG and CDC, and what CNS environmental factors may ...

Current management of neuromyelitis optica (NMO) is noncurative and only partially effective. Immunosuppressive or immunomodulatory agents are the mainstays of maintenance treatment. Safer, better-tolerated, and proven effective treatments are needed. The perceived rarity of NMO has impeded clinical trials for this disease. However, a diagnostic biomarker and recognition of a wider spectrum of ...

Bone morphogenic protein (BMP) signaling is essential for the coordinated assembly of the synapse, but we know little about how BMP signaling is modulated in neurons. Our findings indicate that the Nemo (Nmo) kinase modulates BMP signaling in motor neurons. nmo mutants show synaptic structural defects at the Drosophila melanogaster larval neuromuscular junction, and providing Nmo in motor neuro...

Hinson et al. (1) suggested a unique mechanism for the pathogenesis of neuromyelitis optica (NMO), a neuroinflammatory disease caused by binding of an autoantibody (NMO-IgG) to aquaporin-4 (AQP4) on astrocyte plasma membranes. AQP4 is expressed as long (called M1) and short (called M23) isoforms, the latter forming orthogonal arrays of particles (OAPs). Hinson et al. (1) reported that M1-AQP4 i...

Neuromyelitis optica (NMO) and systemic inflammatory diseases are not mutually exclusive. Even when other autoantibodies are present, myelitis extending over 3 vertebral segments with NMO-IgG positivity discloses the diagnosis of NMO. We report the case of an isolated myelitis extending over 6 vertebral segments due to neuromyelitis optica (NMO). Despite the absence of optic nerve involvement, ...

T cells from neuromyelitis optica (NMO) patients, which recognize the immunodominant epitope of aquaporin-4, exhibit Th17 polarization and cross-react with a homologous sequence of a Clostridium perfringens adenosine triphosphate-binding cassette transporter. Therefore, this commensal microbe might participate in NMO pathogenesis. We examined the gut microbiome by PhyloChip G3 from 16 NMO patie...

In neuromyelitis optica (NMO), the monoclonal B-cell antibody rituximab is a therapeutic option. Little is known about the course of NMO and the safety of rituximab during pregnancy. In this study, we report the clinical course of a patient with NMO after application of rituximab 1 week before inadvertent conception. Mother and child did not experience any adverse event, and the postpartum deve...

Background and Objective: Neuromyelitis optica (NMO) shares certain features with multiple sclerosis (MS). Similar phenotypes, wide spectrum and the differential prevalence of NMO among ethnic backgrounds pose diagnostic challenges. NMO-IgG antibodies are specific biomarker for NMO and facilitate its differentiation from other demyelinating diseases. This study aimed to assess the frequency of ...

BACKGROUND Neuromyelitis optica (NMO) shows various brain magnetic resonance imaging (MRI) abnormalities with recurrent central nervous system (CNS) attacks, although predominantly affecting the spinal cord and optic nerve. However, NMO with extensive involvement of the brain has infrequently been studied. We investigated the clinical, radiographic features and immunomodulating changes of NMO p...

Neuromyelitis optica (NMO) is thought to be caused by immunoglobulin G autoantibodies (NMO-IgG) against astrocyte water channel aquaporin-4 (AQP4). A recent study (Hinson et al. (2012) Proc Natl Acad Sci USA 109:1245-1250) reported that NMO-IgG inhibits AQP4 water permeability directly and causes rapid cellular internalization of the M1 but not M23 isoform of AQP4, resulting in AQP4 clustering,...