Posts tagged: positive

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

Brain Lesions May Serve as Diagnostic Criteria for Neuromyelitis Optica 2011;19(8):13. A majority of patients with neuromyelitis optica also experience disease-specific brain lesions that could help distinguish neuromyelitis optica from multiple sclerosis. MONTREAL—Imaging studies of patients with neuromyelitis optica (NMO)–spectrum disorders reveal that effects of the aquaporin-4 (AQP4) autoantibody, a marker of the disease, may extend beyond the spinal cord and optic nerve, according to researchers

Failure of Natalizumab to Prevent Relapses in Neuromyelitis Optica Ingo Kleiter, MD; Kerstin Hellwig, MD; Achim Berthele, MD; Tania K?mpfel, MD; Ralf A. Linker, MD; Hans-Peter Hartung, MD; Friedemann Paul, MD; Orhan Aktas, MD; for the Neuromyelitis Optica Study Group Arch Neurol. ?2012;69(2):239-245.

Treatment of neuromyelitis optica: an evidence based review.

Clinical features of neuromyelitis optica in a large Japanese cohort: comparison between phenotypes. J Neurol Neurosurg Psychiatry

INTRODUCTION: The existence of antibodies to aquaporin-4 (AQP-4-ab) has identified neuromyelitis optica (NMO) and multiple sclerosis (MS) as different diseases. Although HLA-DRB1 alleles contribute to MS risk, recent studies suggest that HLA back-ground differs between patients with NMO or MS in non-Caucasians populations

Since the description of the association between neuromyelitis optica (Devic’s disease) and aquaporin 4 IgG antibody (NMO-IgG), the search for this antibody has been considered a highly recommended laboratory test when centromedullary multisegmental lesions are observed by magnetic resonance imaging (MRI). Such MRI lesions have not been confined to acute NMO because other infectious and post-infectious disorders may display a similar lesional pattern. However, NMO-IgG has not been currently searched and associated with these myelitides

The autoantibody to aquaporin-4 (AQP4) is a marker and a pathogenetic factor in Neuromyelitis Optica (NMO) (Devic’s syndrome). Our aim was to identify B-cell antigenic linear epitopes of the AQP4 protein and investigate similarities with other molecules. To this end, we screened sera from 21 patients positive for anti-AQP4 antibodies (study group), from 23 SLE and 23 pSS patients without neurologic involvement (disease controls) and from 28 healthy individuals (normal controls)

Background: Neuromyelitis Optica (NMO) serology is a powerful tool for differential diagnosis from Multiple Sclerosis (MS). This study aims to perform a post-marketing evaluation of the first indirect immunofluorescence assay (IIFA) commercially available for NMO serology

In 2004, a highly disease-specific autoantibody named NMO-IgG was discovered in patients with neuromyelitis optica (NMO) and NMO related diseases (i.e. relapsing optic neuritis and longitudinally extensive transverse myelitis). The target antigen of NMO-IgG was identified as aquaporin-4 (AQP4), the main water channel protein in the central nervous system (CNS).

Devic’s neuromyelitis optica is an inflammatory demyelinating disorder normally restricted to the optic nerves and spinal cord. Since the identification of a specific autoantibody directed against aquaporin 4, neuromyelitis optica-immunoglobulin G/aquaporin 4 antibody, neuromyelitis optica has been considered an entity distinct from multiple sclerosis

BACKGROUND: Anti-aquaporin-4 (AQP4) antibody targets perivascular astrocyte foot processes, which contain abundant angiotensinogen, a precursor of angiotensin II, angiotensin-converting enzyme (ACE) and ACE2. OBJECTIVE: To disclose any abnormality in the intrathecal angiotensin II metabolic pathway in Japanese patients with neuromyelitis optica (NMO) or NMO spectrum disorders (NMOs) and positive for anti-AQP4 antibody.