Evaluation of a Multiparametric Immunofluorescence Assay for Standardization of Neuromyelitis Optica Serology Letizia Granieri,#1,2,* Fabiana Marnetto,#1,2 Paola Valentino,1,2 Jessica Frau,3 Agata Katia Patanella,4 Petra Nytrova,5 Patrizia Sola,6 Marco Capobianco,1 Sven Jarius,7 and Antonio Bertolotto1,2 Author information ? Article notes ? Copyright and License information ? Go to: Abstract.
Abstract OBJECTIVE: Neuromyelitis optica spectrum disorder (NMOsd) is an inflammatory and demyelinating syndrome characterized by optic neuritis and myelitis. Several magnetization transfer MRI studies have revealed abnormalities in normal-appearing gray matter in NMOsd. The aim of this study is to elucidate the characteristics and pathogenesis of cognitive impairment and neurodegeneration in NMOsd brains
Impaired regulatory function and enhanced intrathecal activation of B cells in neuromyelitis optica: distinct from multiple sclerosis. Quan C, Yu H, Qiao J, Xiao B, Zhao G, Wu Z, Li Z, Lu C. Source Department of Neurology, Huashan Hospital, Shanghai Medical College, Fudan University, Shanghai, China
Aquaporin 4-specific T cells in neuromyelitis optica exhibit a Th17 bias and recognize Clostridium ABC transporter. Varrin-Doyer M, Spencer CM, Schulze-Topphoff U, Nelson PA, Stroud RM, C Cree BA, Zamvil SS.
Anti-aquaporin-4 antibody in Chinese patients with central nervous system inflammatory demyelinating disorders. Long Y, Qiu W, Hu X, Peng F, Lu Z, Wang Y, Yang Y. Source Department of Neurology, The Third Affiliated Hospital of Sun Yat-Sen University, 600 Tianhe Road, Guangzhou 510630, Guangdong Province, People’s Republic of China; Department of Neurology, Clinical College, The First Affiliated Hospital of Guangdong Pharmaceutical University, 19 Nonglinxia Road, Guangzhou 510080, Guangdong Province, People’s Republic of China.
Atypical presentations of neuromyelitis optica Douglas SatoI, II; Kazuo FujiharaIII IDepartment of Neurology, Tohoku University Graduate School of Medicine, Sendai, Japan IIDepartment of Neurology, Faculty of Medicine – University of São Paulo, São Paulo SP, Brazil IIIDepartment of Multiple Sclerosis Therapeutics, Tohoku University Graduate School of Medicine, Sendai, Japan Neuromyelitis optica (NMO) or Devic’s disease is an inflammatory disease of central nervous system classically characterized by acute, severe episodes of optic neuritis (ON) and longitudinally extensive transverse myelitis (TM)1. The article published in 1894 by Dr Eugène Devic was based on a 45-years old female patient presenting with bilateral ON followed by TM and she deceased about a month after the monophasic opticomyelitis2.
Diagnostic utility of NMO/AQP4-IgG in evaluating CNS inflammatory disease in Thai patients. Apiwattanakul M, Asawavichienjinda T, Pulkes T, Tantirittisak T, Hemachudha T, Horta ES, Jenkins SM, Pittock SJ. Source Department of Neurology, Prasat Neurological Institute, Bangkok, Thailand
J Neuroophthalmol. 2011 Dec 6
Research Contrasting disease patterns in seropositive and seronegative neuromyelitis optica: A multicentre study of 175 patients.
Anti-Aquaporin-4 monoclonal antibody blocker therapy for neuromyelitis optica. Tradtrantip L , Zhang H , Saadoun S , Phuan PW , Lam C , Papadopoulos MC , Bennett JL , Verkman AS . Source Departments of Medicine and Physiology, University of California, San Francisco, CA
Plasma Exchange in Severe Attacks of Neuromyelitis Optica Mickael Bonnan 1 and Philippe Cabre 2 1 Service de Neurologie, Hopital F.
Sudhakar Reddy Kalluri 1 , Veit Rothhammer 1 , Ori Staszewski 2 , Rajneesh Srivastava 1 , Franziska Petermann 1 , Marco Prinz 2 , Bernhard Hemmer 1 , Thomas Korn 1 * 1 Department of Neurology, Klinikum rechts der Isar, Technische Universit?t M?nchen, M?nchen, Germany, 2 Department of Neuropathology, Institute of Pathology, Universit?tsklinikum Freiburg, Freiburg, Germany Abstract? Background Antibodies to the water channel protein aquaporin-4 (AQP4), which is expressed in astrocytic endfeet at the blood brain barrier, have been identified in the serum of Neuromyelitis optica (NMO) patients and are believed to induce damage to astrocytes. However, AQP4 specific T helper cell responses that are required for the generation of anti-AQP4 antibodies and most likely also for the formation of intraparenchymal CNS lesions have not been characterized.