Posts tagged: protein

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

Unlike other mammalian AQPs, multiple tetramers of AQP4 associate in the plasma membrane to form peculiar structures called Orthogonal Arrays of Particles (OAPs), that are observable by freeze-fracture electron microscopy (FFEM). However, FFEM cannot give information about the composition of OAPs of different sizes, and due to its technical complexity is not easily applicable as a routine technique. Recently, we employed the 2D gel electrophoresis BN-SDS/PAGE that for the first time enabled the biochemical isolation of AQP4-OAPs from several tissues.

In neuromyelitis optica (NMO), B-cell autoimmunity to aquaporin-4 (AQP4) has been shown to be essential. However, the role of T cells remains ambiguous

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)

We retrospectively analyzed and compared patterns of anti-aquaporin-4 (AQP4) immunoreactivity of autopsied brains of 2 patients with classical multiple sclerosis (MS) and 2 patients with neuromyelitis optica (NMO). Serological examination for NMO-IgG was not performed in all the cases. We confirmed that the expression of AQP4 is strongly inhibited in demyelinating lesions of NMO, accompanied by the loss of grial fibrillary acidic protein (GFAP) expression

Multiple sclerosis (MS) is a demyelinating disease of the central nervous system (CNS) while neuromyelitis optica (NMO) is an inflammatory disease of the CNS that selectively affects the optic nerves and spinal cord. In Asians, MS is rare; however, when it appears, the selective and severe involvement of the optic nerves and spinal cord is characteristic. This form, termed opticospinal MS (OSMS), has similar features to the relapsing form of NMO in Western populations

We report a 25-year-old woman who developed optic neuritis and encephalomyelitis following primary Sjogren’s syndrome (SjS).

Neuromyelitis optica (NMO) is an inflammatory autoimmune demyelinating disease of the central nervous system (CNS) which in autoantibodies produced by patients with NMO (NMO-IgG) recognize a glial water channel protein, Aquaporin-4 (AQP4) expressed as two major isoforms, M1- and M23-AQP4, in which the plasma membrane form orthogonal arrays of particles (OAPs). AQP4-M23 is the OAP-forming isoform, whereas AQP4-M1 alone is unable to form OAPs.

Neuromyelitis optica (NMO) is an inflammatory disease mainly affecting the optic nerve and spinal cord.

Neuromyelitis optica (NMO) is an inflammatory demyelinating disease with generally poor prognosis that selectively targets optic nerves and spinal cord. Although diagnostic criteria for NMO are available, there is still a need for biomarkers, predicting disease development and progression to improve individually tailored treatment. CSF proteins were separated by two-dimensional electrophoresis and identified by matrix assisted laser desorption ionization time-of-flight mass spectrometry (MALDI-TOF MS)

Neuromyelitis optica (NMO)-immunoglobulin G (IgG) is a clinically validated serum biomarker that distinguishes relapsing central nervous system (CNS) infl ammatory demyelinating disorders related to NMO from multiple sclerosis.

Objective: To analyse clinicoepidemiological features of neuromyelitis optica in a large cohort and to compare the differences between onset age, gender and clinical phenotypes. Methods: Antiaquaporin-4 antibody (AQP4-ab) levels were tested in 2366 serum samples of patients diagnosed as having central nervous system inflammatory demyelinating disorders by their referring physicians. AQP4-ab was measured by indirect immunofluorescence staining using human AQP4-transfected HEK 293 cells.