Neuromyelitis Optica

Matiello, Marcelo; Weinshenker, Brian G.

doi:10.1016/b978-1-4160-6068-0.00013-9

Cited by 14 publications

(23 citation statements)

References 64 publications

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“…In MS, demyelination is characterized by inter-individual rather than intra-individual heterogeneity, with four distinct patterns of focal demyelination identified histologically in biopsy and autopsy samples. Neuromyelitis optica (NMO) is an idiopathic inflammatory demyelinating disease of the CNS that predominantly affects the optic nerves and the spinal cord (Matiello et al, 2007). NMO is a severe monophasic syndrome characterized by bilateral optic neuritis and myelitis that occur in rapid succession.…”

Section: Introductionmentioning

confidence: 99%

Proteomics comparison of the sera from multiple sclerosis patients and neuromyelitis optica patients

Jiang¹,

Lu²,

Hu³

et al. 2014

Genet. Mol. Res.

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ABSTRACT. This study aimed to identify the proteins that are differentially expressed in sera of multiple sclerosis (MS) patients, neuromyelitis optica (NMO) patients, and normal controls by using a two-dimensional gel electrophoresis (2-DE) assay. Serum samples were collected from the 3 groups, and total proteins were isolated and quantified by using the Bradford assay. The 2-DE and silver staining were carried out, and the Image Master 2D Platinum 5.0 software was used to analyze the images. Differentially expressed protein spots were removed from the gel and digested by enzymolysis and high-definition tandem mass spectrometry, and the MASCOT online software was applied to identify the proteins. Three differentially expressed proteins were identified: immunoglobulin (Ig) lambda chain, keratin 83, and haptoglobin (Hp2); the Ig lambda chain was only found in MS patients. The expression of keratin 83 was significantly elevated in the MS group compared to the normal control or NMO groups. The expression of Hp2 in the NMO group was elevated by more than 2-fold compared to the normal control or MS groups. In summary, a variety of proteins were found to be differentially expressed in the serum between MS, NMO, and normal subjects using 2-DE: Ig lambda, Hp2, and keratin 83 were identified as potential diagnostic markers or treatment targets for MS or NMO.

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Section: Introductionmentioning

confidence: 99%

Proteomics comparison of the sera from multiple sclerosis patients and neuromyelitis optica patients

Jiang¹,

Lu²,

Hu³

et al. 2014

Genet. Mol. Res.

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“…78 Relapsing NMO is more common than monophasic disease. 15,79,80 The onset of disease is later than in MS; it typically starts in the late 30 s. 79,81,82 Relapsing NMO is about five times more frequent among females, although highly variable in different cohorts. 80,82 Female gender is a strong independent predictor of a relapsing course.…”

Section: Epidemiology Of Nmomentioning

confidence: 99%

“…Several other diseases should be also considered, depending on the clinical presentation and medical history, including systemic autoimmunity and LHON. 15,54,63,102 Myelitis Several aspects should be considered; isolated or relapsing, longitudinally extending or partial, and the presence of other symptoms ⁄ signs. In any case of LETM, screening for anti-AQP4 antibodies is necessary (Fig.…”

Section: Relapsing or Bilateral Optic Neuritismentioning

confidence: 99%

“…8,9 Outside the CNS, AQP4 is expressed in skeletal muscles, distal collecting tubules of the kidney, parietal cells of the stomach, colon epithelium, tracheal and bronchial epithelium, and glandular epithelia of breast and salivary glands. 10,11 Several data show that anti-AQP4 antibodies are pathogenic: (i) antibodies binding to AQP4 are present in a substantial portion of patients with NMO; (ii) NMO-IgG titers in sera might correlate with clinical disease activity; 6,12 (iii) in CNS plaques of NMO characterized by antibody and complement deposition, AQP4 molecules are absent in contrast to MS, 6,[14][15][16] and glial fibrillary acidic protein (GFAP) (an astrocyte marker) immunoreactivity is lost along with increased cerebrospinal fluid (CSF) levels of soluble GFAP; [17][18][19] (iv) sera containing NMO-IgG induces complement-dependent necrosis of astrocytes in vitro; [20][21][22][23][24] (v) human NMO sera recognize an extracellular epitope of AQP4 and induce AQP4 endocytosis in transfected cell lines. 17,20,21,23,25,26 The third extracellular loop of AQP4 might be the major epitope for antibodies in NMO; 27 (vi) IgG isolated from sera or recombinant antibodies generated from CSF of NMO patients were able to transfer disease.…”

Section: Introductionmentioning

confidence: 99%

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Pathogenesis, diagnosis and treatment of neuromyelitis optica: Changing concept of an old disease

Illés

2010

Clinical & Exp Neuroim

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The concept of neuromyelitis optica (NMO) has changed considerably during the past few years. The identification of autoantibodies in the sera generated against the water channel aquaporin 4 (AQP4) has increased the specificity of diagnosis and modified guidelines. A pathogenic role of anti‐AQP4 antibodies has recently been indicated; they evoke the pathological and clinical hallmarks of the disease on transfer and cause necrosis of astrocytes expressing AQP4. The diagnosis of NMO is based on clinical, neuroimaging and serological criteria. Early therapy preventing relapses is mandatory, because neurological impairment accumulated during relapses is the main cause of permanent disability. In a number of cases defined as NMO spectrum diseases, the clinical manifestation is spatially limited. Such events of separate myelitis or relapsing/bilateral optic neuritis challenge diagnosis and might delay proper therapy. Here, current concepts of diagnosis and treatment of NMO and NMO spectrum diseases are summarized. Diagnostic and treatment decisions in different clinical situations are shown by discussion of cases. (Clin. Exp. Neuroimmunol. doi: 10.1111/j.1759‐1961.2010.00011.x, 2010)

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“…Only in 2004, NMO had been recognized as a unique demyelinating disease 8 when Lennon et al 9 identified a serum autoantibody marker in patients with NMO, named NMO-IgG (AQP4-IgG), that bound selectively to the aquaporin 4 (AQP4) water channels which is concentrated in the astrocytic foot processes at the blood-brain barrier. It would be not merely a marker but a causative agent 10 .…”

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confidence: 99%