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Disease Info Card
Neuromyelitis Optica
Information about Neuromyelitis Optica: characteristics, related genes and pathways, plus antibodies you can use for research. This page is being enriched constantly, if you see some information you would like this page to include please send your suggestions to us.
Overview of Neuromyelitis Optica
Most recent studies have shown that Neuromyelitis Optica shares some biological mechanisms with autoimmune-diseases, autoimmune-reaction, blind-vision, cns-disorder, demyelinating-diseases, demyelination, disorder-of-the-optic-nerve, encephalomyelitis, encephalomyelitis-acute-disseminated, inflammation, multiple-sclerosis, myelitis, myelitis-transverse, nervous-system-disorder, nervousness, neuritis, optic-neuritis, sclerosis, spinal-cord-diseases.
Among the many pathways, these few ones have gauged particular interests from scientists studying Neuromyelitis Optica, and have been seen in publications frequently: B Cell Activation, Cell Activation, Cell Death, Cell Migration, Cell Proliferation, Complement Activation, Complement-dependent Cytotoxicity, Cytokine Production, Glutamate Homeostasis, Humoral Immune Response, Immune Response, Inflammatory Response, Localization, Pathogenesis, Reflex, Secretion, T Cell Activation, Translation, Transport, Water Transport
Quite a number of genes have been found to play important roles in Neuromyelitis Optica, such as ALB, AQP4, CSF2, FANCA, GFAP, HLA-DRB1, HLA-DRB4, IFNB1, IL17A, IL6, KRT20, LAMC2, MAG, MBL2, MBP, MOG, MS4A1, PRG2. See what Boster has to offer for the research of these genes by clicking the gene name links below and view a more detailed info card/product listing for that gene.
In a later update, we will include information such as current drugs and therapy solutions as well as on-going and past clinical trials for this disease. Plesae stay updated.