73 results about "Demyelinated diseases" patented technology

The present invention provides methods and compositions for the production of glial cells and oligodendrocytes from placenta stem cells. The invention further provides for the use of these glia and oligodendrocytes in the treatment of, and intervention in, for example, trauma, ischemia and degenerative disorders of the central nervous system (CNS), particularly in the treatment of demyelinating diseases such as multiple sclerosis.

Disclosed are NgR proteins and biologically active Nogo (ligand) protein fragments. Also disclosed are compositions and methods for modulating the expression or activity of the Nogo and NgR protein. Also disclosed are peptides which block Nogo-mediated inhibition of axonal extension. The compositions and methods of the invention are useful in the treatment of cranial or cerebral trauma, spinal cord injury, stroke or a demyelinating disease.

Antibodies, and particularly human antibodies, are disclosed that demonstrate activity in the treatment of demyelinating diseases as well as other diseases of the central nervous system that are of viral, bacterial or idiopathic origin, including neural dysfunction caused by spinal cord injury. Neuromodulatory agents are set forth that include and comprise a material selected from the group consisting of an antibody capable of binding structures or cells in the central nervous system, a peptide analog, a hapten, active fragments thereof, agonists thereof, mimics thereof, monomers thereof and combinations thereof. The neuromodulatory agent has one or more of the following characteristics: it is capable of inducing remyelination; binding to neural tissue; promoting Ca−− signaling with oligodendrocytes; and promoting cellular proliferation of glial cells. Amino acid and DNA sequences of exemplary antibodies are disclosed. Methods are described for treating demyelinating diseases, and diseases of the central nervous system of humans and domestic animals, using polyclonal IgM antibodies and human monoclonal antibodies sHIgm22(LYM 22), sHIgm46(LYM46) ebvHIgM MSI19D10, CB2bG8, AKJR4, CB2iE12, CB2iE7, MSI19E5 and MSI10E10, active fragments thereof and the like. The invention also extends to the use of human antibodies, fragments, peptide derivatives and like materials, and their use in diagnostic and therapeutic applications, including screening assays for the discovery of additional antibodies that bind to cells of the nervous system, particularly oligodendrocytes.

The present invention relates to methods of treating or ameliorating certain neurodegenerative disorders (namely, dysmyelinating and demyelinating disorders) in patients in need of such treatment or amelioration. The invention provides methods of treating or ameliorating a patient in need of such treatment and includes the administration to the patient of: (a) thyroid hormones or thyroid hormone analogues; (b) cell replacement therapies involving the use of homogenous Oligodendrocyte Precursor Cells derived from embryonic stem cells that have been treated with thyroid hormones or thyroid hormone analogues; (c) gene therapy to correct mutated genes in vivo; or (d) a combination of two or more of (a), (b) and (c). The invention also provides compositions and formulations of thyroid hormones and thyroid hormone analogues for use in treating or ameliorating such disorders.

Provided is a method of inducing oligodendrocyte precursor cells (OPCS) through direct reprogramming from human somatic cells into which a nucleic acid molecule encoding an Oct4 protein or Oct4 protein-treated human somatic cells. The method of inducing OPCs by treating Oct4-overexpressing human somatic cells with a low molecular weight substance may establish OPCs with high efficiency in a short period of time through direct reprogramming without via neural stem cells, and thus the OPCs are useful as a cell therapeutic agent for an intractable demyelinating disease.

The present invention concerns the diagnosis and treatment of autoimmune demyelinating diseases, such as multiple sclerosis (MS), by means of a CLM-I agonist.

A novel therapeutic agent or prophylactic agent for a demyelinating disease is provided. An amino alcohol derivative represented by the general formula (1),which is a sphingosine-1-phosphate receptor agonist, a pharmacologically acceptable salt or hydrates thereof, are a therapeutic agent or prophylactic agent for a demyelinating disease.

The invention relates to the technical field of biological drug carrier preparation, and particularly discloses a targeting extracellular vesicle as well as a preparation method and application thereof. The method comprises the following steps: constructing an LV-Lc-PDGFA fusion expression lentiviral vector, infecting neural stem cells, constructing a stably transfected cell line NSC-LV-Lc-PDGFA, and positioning an expressed exogenous ligand PDGFA on the surface of an extracellular vesicle membrane, so that the targeting capability of the extracellular vesicles on the oligodendroglia lineage cells is improved. The extracellular vesicle with the membrane surface expressing the PDGFA small peptide has high targeting property, can be used as a drug carrier, and has a good treatment effect on demyelination diseases.

The present invention relates generally to methods of using nalmefene for treating and / or preventing demyelinating disease in a subject, and in particular for treating and / or preventing multiple sclerosis (MS). Also disclosed is nalmefene for use in treating and / or preventing MS as well as pharmaceutical compositions and unit dosage forms comprising nalmefene for use for treating and / or preventing demyelinating disease in a subject, and in particular for treating and / or preventing MS.

Provided is a method of inducing oligodendrocyte precursor cells (OPCs) through direct reprogramming from human somatic cells into which a nucleic acid molecule encoding an Oct4 protein or Oct4 protein-treated human somatic cells. The method of inducing OPCs by treating Oct4-overexpressing human somatic cells with a low molecular weight substance may establish OPCs with high efficiency in a short period of time through direct reprogramming without via neural stem cells, and thus the OPCs are useful as a cell therapeutic agent for an intractable demyelinating disease.

The present invention relates to methods and pharmaceutical compositions for treating peripheral demyelinating diseases. In particular the present invention relates to a method of treating a peripheral demyelinating disease in a subject in need thereof comprising administering to the subject a therapeutically effective amount of an inhibitor of VDAC1 activity or expression.

The present invention concerns a method for treating a demyelinating condition in a subject, by administering an agent to the subject that inhibits vascular endothelial cell phagocytosis. The method of the invention is useful in treating, for example, a demyelinating condition associated with an injury, such as a spinal cord injury or traumatic brain injury, as well as other demyelinating conditions, such as multiple sclerosis.

The invention provides a pharmaceutical composition for treating central nervous system inflammatory demyelinating diseases. The pharmaceutical composition comprises 2-(2-benzofuranyl)-2-imidazoline or a pharmaceutically acceptable salt, a hydrate and a solvate thereof as an active ingredient, and 7-(2-phenylethyl)-5-amino-2-(2-furyl)-pyrazolo-(4, 3-e)-1, 2, 4-triazolo (1, 5-c) pyrimidine or a pharmaceutically acceptable salt, a hydrate and a solvate thereof. The invention further provides a combination containing two medicaments and also provides application of the pharmaceutical composition and the pharmaceutical combination in combined treatment of the central nervous system inflammatory demyelinating diseases, and the synergistic treatment effect is obtained.

The present invention is concerned with deuterium-enriched pyrimidine compounds of formula 1, their derivatives and pharmaceutically acceptable salts and methods of use thereoffor the prevention and treatment of neuroendocrine neoplasia including metastasis and fibrosis, fibrotic processes associated with neuroendocrine cell dysregulation for example Crohn's disease, pulmonary arterial hypertension, pulmonary hypertension associated with chronic obstructive pulmonary disease (COPD), right ventricular hypertrophy, pulmonary vascular remodeling, asthma, cystic fibrosis, hypertension, ischemic stroke, angina pectoris, congestive heart failure, arrhythmia, arterial fibrillation, neurodenerative diseases, gastrointestinal disorders , stress disorders, obsessive compulsive disorders, demyelinating diseases, cereberal vascular disorders, bronchoconstriction, vasodilation, smooth muscle contraction, brain disorders, vascular disorders, neuropathological diseases and cardiovascular system regulation.

The invention discloses a construction method of a transgenic fish (mbp:egfp) demyelinating disease model established by using a drug scopoletin, and the method comprises the following steps: placing the transgenic fish (mbp:egfp) in a 18.5 [mu] g / ml scopoletin solution, and completing the construction of a zebra fish model after 3-6 days. By combining various factors such as genes, environment, aging and the like, the zebrafish demyelination disease model can be quickly constructed, and a basis is provided for a mechanism and a treatment method of the demyelination disease.

The invention belongs to the technical field of biological medicine, and particularly relates to a single-domain antibody VHH-L1 targeting LINGO-1 protein, and the amino acid sequence of the single-domain antibody VHH-L1 is shown as SEQ ID NO: 1. The single-domain antibody has nanomole-level high affinity and excellent specificity, can effectively block the interaction between LINGO-1 and ligands thereof, and remarkably promotes differentiation and myelination of oligodendroglia cells. The invention further provides a neural stem cell subjected to genetic engineering modification, and the neural stem cell can stably and continuously secrete the single-domain antibody VHH-L1. In a spinal cord injury animal model, the engineered stem cell shows an excellent treatment effect, can significantly promote motor function recovery, axon regeneration and myelin sheath repair, and effectively inhibits glial scar formation. The double advantages of cell therapy and long-acting protein delivery are fused, and a brand new efficient treatment strategy is provided for demyelination diseases such as multiple sclerosis and spinal cord injury.

A method for determination of an indicator representative of a change in the brain caused by a demyelinating disease, the method including, for each region of interest of the brain, determining a regional coefficient of one of the following diffusion coefficients: the radial diffusion, the axial diffusion, the mean diffusion, the anisotropy fraction, or a combination of several of these coefficients, the regional coefficients being determined from a diffusion MRI image; determining a number of changed regions, for which a condition relating to the value of the regional diffusion coefficient of each region is satisfied; and determining the indicator in accordance with the number of changed regions.

The invention belongs to the technical field of medicines, and discloses application of a compound M1 shown as a formula (I) and pharmacodynamically acceptable salt thereof in preparation of medicines for preventing, relieving and / or treating autoimmune demyelination diseases. On a mouse experimental autoimmune encephalomyelitis model, the compound M1 shows a good treatment effect, can effectively prevent and treat pathological changes and disease progression of diseases, relieve the severity of the diseases and inhibit LPS-stimulated microglial BV2 cells from releasing inflammatory mediators, and provides a new drug and a new structure for clinical treatment.

The present invention provides methods and compositions for treating a CNS disease, disorder or injury, (e.g., a CNS demyelinating disease). The present invention provides methods and compositions for preserving or protecting neuroaxonal activity in a subject, preferably a mammalian subject (e.g., a human) by administering one or more compositions that inhibit the activity of γ-glutamyl transpeptidase in the human subject.

CC chemokine mutants contain at least two mutations at the cationic site of the 40’S loop (40’s loop), which have lower GAG-binding activity compared with the wild-type molecule. In particular, the present inventors have shown that these mutated chemokines are effective in the treatment of multiple sclerosis and / or other demyelinating diseases. The RANTES triple mutant was the most effective compound.

The present disclosure provides a three-dimensional culture system comprising a biocompatible polymer and a combination of factors in an amount effective to induce differentiation of oligodendrocyte precursors and / or oligodendrocytes from pluripotent stem cells. The present disclosure provides methods of generating oligodendrocyte precursors and / or oligodendrocytes using a three-dimensional culture system of the present disclosure. The present disclosure provides methods to treat neurological diseases and demyelinating diseases.

The present invention relates generally to methods of using nalfurafine for treating and / or preventing demyelinating disease in a subject, and in particular for treating and / or preventing multiple sclerosis (MS). Also disclosed is nalfurafine for use in treating and / or preventing MS as well as pharmaceutical compositions and unit dosage forms comprising nalfurafine for use for treating and / or preventing demyelinating disease in a subject, and in particular for treating and / or preventing MS.

This invention provides novel methods for treating or ameliorating symptoms of demyelinating diseases such as multiple sclerosis. The methods involve administering to subjects in need of treatment a pharmaceutical composition that contains a therapeutically effective amount of taurine and also a compound that induces oligodendrocyte precursor cell (OPC) differentiation (e.g., T3, benztropine, clemastine or miconazole). Some of the methods additionally involve administration to the subject a known agent for treating demyelinating diseases (e.g., SIP receptor agonists) or a known disease modifying drug. The invention also provides methods for increasing myelination and methods for promoting OPC differentiation into oligodendrocytes. These methods entail contacting a population of OPCs with a combination of taurine and a known OPC differentiation-inducing agent such as T3, clemastine, benztropine or miconazole.

The invention provides a means for a treatment for a demyelinating disease of the central nervous system (CNS) characterized by the presence of an anti-myelin oligodendrocyte glycoprotein (MOG) antibody, and also for reducing the risk of relapse in the demyelinating disease, comprising an anti-IL-6 receptor antibody or antigen binding fragment thereof.

The invention discloses a deep fusion learning-based child brain MRI demyelination auxiliary analysis method. The method comprises the following steps of: firstly, preprocessing child demyelination disease data and constructing a data set; designing a deep fusion learning demyelination disease auxiliary model; training the deep fusion learning demyelinating disease auxiliary model through the constructed child demyelinating disease data set; and finally, completing acquisition and feature classification of a high-signal white matter segmentation image through the trained deep fusion learning demyelination disease auxiliary model, and displaying the high-signal white matter segmentation image and a feature classification label through a visual result model. The method provided by the invention not only can assist doctors in clinical diagnosis, but also can greatly improve the rate of image annotation, so that the definite diagnosis time and definite diagnosis cost of patients are greatly shortened and reduced, the patients can be treated in time, neurological function defects left in the prognosis process of the patients are relieved, and a better prognosis effect is obtained.

The present disclosure provides compounds ("PDGFR [alpha] inhibitors") that can specifically target PDGFR [alpha], and thus reduce and / or inhibit the activation of the receptor. The present disclosure also provides methods of treating demyelinating disease using the disclosed PDGFR [alpha] inhibitors.

The present application relates generally to the field of bone morphogenetic protein (BMP) antagonists (soluble ALK6 fusion proteins), compositions thereof, and methods for treating degenerative and / or demyelinating diseases of the nervous system.

The present invention provides novel imidazolopyrazine compounds, compositions and methods for treating or preventing an IRE1α-related disease or disorder. In certain embodiments, the disease or disorder is selected from the group consisting of a neurodegenerative disease, a demyelinating disease, cancer, an eye disease, a fibrotic disease, and diabetes.