38 results about "Neuromyelitis optica" patented technology

The present invention relates to the use of selective aquaporin inhibitors, e.g., of aquaporin-4 or aquaporin-2, e.g., certain phenylbenzamide compounds, for the prophylaxis, treatment and control of aquaporin-mediated conditions, e.g., diseases of water imbalance, for example edema (particularly edema of the brain and spinal cord, e.g., following trauma or ischemic stroke, as well as the edema associated with glioma, meningitis, acute mountain sickness, epileptic seizures, infections, metabolic disorders, hypoxia, water intoxication, hepatic failure, hepatic encephalopathy, diabetic ketoacidosis, abscess, eclampsia, Creutzfeldt-Jakob disease, and lupus cerebritis, as well as edema consequent to microgravity and / or radiation exposure, as well as edema consequent to invasive central nervous system procedures, e.g., neurosurgery, endovascular clot removal, spinal tap, aneurysm repair, or deep brain stimulation, as well as retinal edema), as well as hyponatremia and excess fluid retention, and diseases such as epilepsy, retinal ischemia and other diseases of the eye associated with abnormalities in intraocular pressure and / or tissue hydration, myocardial ischemia, myocardial ischemia / reperfusion injury, myocardial infarction, myocardial hypoxia, congestive heart failure, sepsis, and neuromyelitis optica, as well as migraines, as well as to novel assays for identifying aquaporin inhibitors.

The invention discloses a detection method of an aquaporin-4 autoantibody, a fusion expression virus vector and application thereof. The virus vector is pCDH-MCS-AQP4-EF1-copGFP, the nucleotide sequence of which is shown as a sequence table SEQIDNO.2. The invention further discloses application of the fusion expression virus vector in improving the clinical diagnosis and treatment level of ophthalmoneuromyelitis and multiple sclerosis. By adopting immunofluorescent cytochemical staining with higher sensitivity and specificity combined with a flow cytometric detection technology, the AQP-4 antibody is quantitively and qualitatively detection clinically, so that the detection result is more stable, and the labor and the time cost are extremely saved. The project is established to extremely improve the diagnosis and treatment level of ophthalmoneuromyelitis and multiple sclerosis, so that the labor capacity and the living quality of the patient are improved, and huge social and economic benefits are generated.

The present invention is directed to antibodies binding to aquaporin 4 (AQP4) and methods of using such antibodies to treat neuromyelitis optica (NMO) either as a monotherapy or in combination with standard NMO therapies such as immunosuppressives or plasmaphersis.

The present invention relates to the use of selective aquaporin inhibitors, e.g., of aquaporin-4 or aquaporin-2, e.g., certain phenylbenzamide compounds, for the prophylaxis, treatment and control of aquaporin-mediated conditions, e.g., diseases of water imbalance, for example edema (particularly edema of the brain and spinal cord, e.g., following trauma or ischemic stroke, as well as the edema associated with glioma, meningitis, acute mountain sickness, epileptic seizures, infections, metabolic disorders, hypoxia, water intoxication, hepatic failure, hepatic encephalopathy, diabetic ketoacidosis, abscess, eclampsia, Creutzfeldt-Jakob disease, and lupus cerebritis, as well as edema consequent to microgravity and / or radiation exposure, as well as edema consequent to invasive central nervous system procedures, e.g., neurosurgery, endovascular clot removal, spinal tap, aneurysm repair, or deep brain stimulation, as well as retinal edema), as well as hyponatremia and excess fluid retention, and diseases such as epilepsy, retinal ischemia and other diseases of the eye associated with abnormalities in intraocular pressure and / or tissue hydration, myocardial ischemia, myocardial ischemia / reperfusion injury, myocardial infarction, myocardial hypoxia, congestive heart failure, sepsis, and neuromyelitis optica, as well as migraines, as well as to novel assays for identifying aquaporin inhibitors.

A method for treating demyelinating diseases in a patient in need thereof by treatment with an effective amount of a PPAR delta agonist is disclosed. Demyelinating diseases that may be effectively treated by this method include but are not limited to multiple sclerosis, Charcot-Marie-Tooth disease, Pelizaeus-Merzbacher disease, encephalomyelitis, neuromyelitis optica, adrenoleukodystrophy, Guillian-Barre syndrome and disorders in which myelin forming glial cells are damaged including spinal cord injuries, neuropathies and nerve injury.

The invention relates to the field of application of B lymphocyte stimulating factor acceptor-antibody fusion protein to treatment of autoimmunity diseases, in particular to an application of TACI-Fcfusion protein to preparation of medicines for treating neuromyelitis opticaspectrum disorders (NOOSD) and multiple sclerosis (MS).

The present disclosure provides human Aquaporin 4 (AQP4) peptides and peptides having homology to human Aquaporin 4 (AQP4) peptides. Also provided herein are methods for using human AQP4 peptides and peptides homologous to human AQP4 peptides for diagnosing and / or treating Neuromyelitis Optica.

2-Chloro-2′-deoxyadenosine, hereinafter referred to as cladribine, or a pharmaceutically acceptable salt thereof may be used in the treatment or amelioration of neuromyelitis optica, hereinafter referred to as NMO e.g. in patients known to have NMO-IgG seropositivity or in patients optic neuritis, myelitis and at least two of MRI evidence of contiguous spinal cord lesion 3 or more segments in length, onset brain MRI nondiagnostic for multiple sclerosis or NMO-IgG seropositivity.

The invention relates to a method of diagnosis of neuromyelitis optica, in particular of differential diagnosis of neuromyelitis optica (NMO) vs. multiple sclerosis (MS) using miRNA biomarkers. These miRNAs could potentially serve as future diagnostic biomarkers for NMO and help in diagnosis, monitoring disease activity, and evaluation of treatment responses in patients with MS.

The invention discloses application of chrysin in preparation of medicaments for treating autoimmune diseases. Experimental results show that the chrysin can inhibit differentiation of human immune dendritic cells (DC) and maturity of LPS (lipopolysaccharide)-activated human immune DC, can inhibit the antigen uptake capabilities of the immature DC and the antigen presenting capabilities of the mature DC and can inhibit T cell proliferation reactions stimulated by the DC. In particular, the chrysin can reduce the average score, the highest score and the total score of clinical scores of experimental autoimmune encephalomyelitis of mice and can relieve myelitis cell infiltration and demyelination in spinal cords. Thus, the medicament inhibiting immune systems is expected to become the medicament for treating such autoimmune inflammatory diseases as multiple sclerosis, neuromyelitis optica and acute disseminated encephalomyelitis clinically.

The present disclosure relates generally to methods of preventing, reducing risk of developing, or treating neuromyelitis optica (NMO) and, more specifically, to methods involving the inhibition of the classical pathway of complement activation.

The invention relates to the use of diazoxide or a pharmaceutically acceptable salt thereof at low doses to treat a CNS autoimmune demyelinating disease selected from selected from multiple sclerosis (MS), clinically isolated syndrome (CIS), tumefactive (tumor-like) M S, Marburg's acute M S, Balós's concentric sclerosis, acute disseminated encephalomyelitis (ADEM), post-vaccinal encephalitis (PVE), post-infectious encephalomyelitis (PIE) and neuromyelitis optica (NMO).

The invention provides a stably transferred cell strain for detecting NMO-IgG (neuromyelitis optica-immunoglobulin G) and a construction method of the stably transfected cell strain. The constructionmethod comprises steps as follows: an overexpression vector containing an AQP4 M1 gene is constructed, slow viruses are packaged in overexpression vector transfected cells, the slow viruses are concentrated and purified to transduce the cells, antibiotics corresponding to resistance of the vectors act on the transduced cells, and the stably transferred cell strain is obtained by screening. The exogenous genes are integrated to cell chromosomes, so that the constructed stably transferred cell strain can continuously and stably express AQP4 M1 protein for a long time, and the defect of short expression duration of the exogenous genes in instantaneous infection is overcome.

The invention belongs to the technical field of DNA recombination, and discloses a primer, a coded cDNA, a vector, an AQP4 monoclonal antibody, and a preparation method of the AQP4 monoclonal antibody. A cho-cell clone expressing rat AQP4 m23 is established; the cDNA of the encoded rat AQP4 m23 is coned from total RNA extracted from a rat brain through using a primer reverse transcription polymerase chain reaction; and the cDNA is inserted into NheI and SacII sites of a perres 2-egfp vector after sequencing is carried out. The anti-mouse AQP4 and the anti-human AQP4 prepared in the invention have high affinity to AQP4 in the central nervous system in mice, and are proved to induce neuromyelitis optica lesions and symptoms in mice in vitro and in vivo. The studying and new treatment methodexploration of the neuromyelitis optica are benefited.

The present invention is directed to antibodies binding to aquaporin 4 (AQP4) and methods of using such antibodies to treat neuromyelitis optica (NMO) either as a monotherapy or in combination with standard NMO therapies such as immunosuppressives or plasmaphersis.

The invention discloses a biomarker for NMOSD prediction or recurrence monitoring and application of the biomarker. By preparing a reagent or a kit capable of detecting and analyzing the expression level of the biomarker, the corresponding biomarker in peripheral blood or plasma exosome of a subject is detected, so that the neuromyelitis optica pedigree disease can be predicted and monitored; not only can the onset risk of the neuromyelitis optica pedigree disease of the subject be predicted, but also the recurrence of the neuromyelitis optica pedigree disease of the patient or the subject can be monitored. The present invention provides the biomarker for NMOSD prediction or recurrence monitoring, which is helpful to better understand the pathophysiology of NMOSD, thereby improving clinical service for NMOSD patients.

The present invention provides pharmaceutical compositions for treating neuromyelitis optica (NMO) comprising a therapeutically effective amount of loop C sequence-containing peptide of aquaporin-4 (AQP4) water channel, or a therapeutically effective fragment or variant thereof. The invention also provides methods for treating NMO by administering therapeutically effective amounts of loop C sequence-containing peptide(s) of AQP4, optionally in an immunosuppressive setting, and also provides diagnostics for detection of NMO in a subject, screening methods for identification of NMO-treating therapeutics and NMO model systems.

Provided herein are methods and compositions for treating inflammatory diseases by administering to the subject an effective dose of an anti-alpha5 agent. Specifically, the methods are provided for the treatment of inflammatory diseases, including neuroinflammatory disease such as, neuroinflammatory demyelinating autoimmune diseases including multiple sclerosis (MS) and neuromyelitis optica (NMO),as well as the treatment of amyotrophic lateral sclerosis (ALS).

The invention relates to the use of diazoxide or a pharmaceutically acceptable salt thereof at low doses to treat a CNS autoimmune demyelinating disease selected from selected from multiple sclerosis (MS), clinically isolated syndrome (CIS), tumefactive (tumor-like) MS, Marburg's acute MS, Bal?s's concentric sclerosis, acute disseminated encephalomyelitis (ADEM), post-vaccinal encephalitis (PVE), post-infectious encephalomyelitis (PIE) and neuromyelitis optica (NMO).

Neutrophils contribute to demyelinating autoimmune diseases, yet their phenotype and functions have been elusive to date. The present application shows that ICAM1 surface expression distinguishes extra- from intravascular neutrophils. Transcriptomic analysis of these two subpopulations indicated that neutrophils, once extravasated, acquire macrophage-like properties, including the potential for immunostimulation and MHC class II-mediated antigen presentation. Further, the present application shows that aspartic retroviral-like protease ASPRV1 is specifically expressed by neutrophils in the mouse and human immune system, and correlates with CNS neutrophil infiltration in EAE, multiple sclerosis and neuromyelitis optica.

An ELISpot diagnosis kit for NMO and its application are characterized in that, the polypeptide fragment specific to NMO effector T-cell is obtained through topological conformation analysis of aquaporin-4 (AQP-4), followed by the structural analyses of the related polypeptides after combination and rearrangement so as to screen out the brand-new polypeptide fragment suitable for NMO disease diagnosis. In the ELISpot experiment, by utilizing the obtained polypeptide fragment, stimulate the effector T-cell in the NMO disease to secrete IL-4, proving the feasibility and scientific value of that polypeptide fragment in the NMO diagnosis. This method is with strong specificity, high sensitivity and easy operations, and it can be developed into the diagnosis kit for the diagnosis and differential diagnosis of NMO in the clinical examination, laying the foundation for the early discovery and treatment of NMO.

The invention discloses a film strip for typing neuromyelitis optica pathopoiesis autoantibodies. The film strip comprises an NMO-IgG typing film strip. Small peptides A, C and E are adsorbed to the NMO-IgG typing film strip. The amino acid sequence of the small peptide A is TINWGGTEKPLPVDMV from the end N to the end C. The amino acid sequence of the small peptide C is CVTPPSVVGGLGVTTVHGNLTAG fromthe end N to the end C. The amino acid sequence of the small peptide E is INYTGASMNPARSFGPAVIMGNWENHW from the end N to the end C. The film strip for typing the neuromyelitis optica pathopoiesis autoantibodies can accurately type NMO-IgG in body fluids of NMO patients and clinically assists in accurate diagnosis, and accordingly, appropriate treatment is achieved. Currently, the typing method isproposed for the first time internationality and domestically, and has obvious progressive significance.

The present invention relates to a method for the diagnosis and / or risk stratification of neuromyelitis optica (abbreviated NMO), wherein a determination from a body sample of a patient / test subject is performed by means of artificial aquaporin-4 peptides. The invention further relates to a kit and to new artificial aquaporin-4 peptides as such.

The invention relates to the use of biotin for treating Amyotrophic Lateral Sclerosis, as well as demyelinating peripheral neuropathies and Neuromyelitis optica (NMO).

Methods of clinical treatment of neuromyelitis optica lineage disorder (NMOSD) using anti-C5 antibodies or antigen-binding fragments thereof are provided.

An ELISpot diagnosis kit for NMO and its application are characterized in that, the polypeptide fragment specific to NMO effector T-cell is obtained through topological conformation analysis of aquaporin-4 (AQP-4), followed by the structural analyses of the related polypeptides after combination and rearrangement so as to screen out the brand-new polypeptide fragment suitable for NMO disease diagnosis. In the ELISpot experiment, by utilizing the obtained polypeptide fragment, stimulate the effector T-cell in the NMO disease to secrete IL-4, proving the feasibility and scientific value of that polypeptide fragment in the NMO diagnosis. This method is with strong specificity, high sensitivity and easy operations, and it can be developed into the diagnosis kit for the diagnosis and differential diagnosis of NMO in the clinical examination, laying the foundation for the early discovery and treatment of NMO.

The present invention is directed to stimulate the neuroregeneration of the central nervous system due to autoimmune damage. In particular the pharmaceutical combination that comprise therapeutically effective concentrations of the Epidermal Growth Factor and the Growth Hormone Releasing Peptide-6, is administrated to a subject that suffers from symptoms of Multiple Sclerosis and Optic Neuromyelitis and corrects the demyelination caused by autoreactive cells in central nervous system.