88 results about "Demyelinations" patented technology

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 application belongs to the technical field of medicine, and particularly relates to application of echinacoside in preparation of a medicine for preventing or treating a demyelination disease; the echinacoside can promote differentiation and maturation of OPCs to OLs, promote proliferation of OLs, promote myelin repair, improve pathological changes of myelin ultrastructure, and promote myelin thickness to return to a normal level; the scheme provides a new treatment means for preventing or treating the demyelination disease, and is expected to reverse disability caused by myelin shedding or damage.

This invention provides the use of a trisaccharide compound with a core structure of GlcN(1→4)IdoA(1→4)GlcNS in the preparation of a medicament for the treatment or prevention of multiple sclerosis. The compound can delay the onset of clinical symptoms in patients, reduce or alleviate or improve patients' clinical symptoms and signs, improve or inhibit nerve demyelination, and improve or inhibit inflammation of the central nervous system.

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 disclosure provides methods for (i) treating multiple sclerosis in patient, (ii) treating a patient having symptoms of multiple sclerosis, (iii) preventing the onset of multiple sclerosis symptoms in patient having multiple sclerosis or predisposed to multiple sclerosis; (iv) promoting or enhancing immunomodulation and remyelination and / or myelin repair in a subject in need thereof; (v) a neuroinflammatory disorder; (vi) Amyotrophic Lateral Sclerosis; or (vii) a demyelinating disease or disorder or a hypomyelinating condition, each method comprising administering a therapeutically effective amount of a bryostatin compound to the patient.

The invention relates to the technical field of new application of medicines, in particular to application of G15 to treatment of white matter injury based on promotion of cerebrovascular generation, and finds that the G15 has the effect of promoting cerebrovascular generation, can promote myelination insufficiency caused by hypoxia in the early development stage and can improve neurological dysfunction caused by hypoxia, and the G15 has the effect of promoting cerebrovascular generation. Moreover, myelin sheath regeneration of a local demyelination area after the adult can be promoted, so that the effect of directly treating the white matter injury from the pathological aspect is achieved. The invention provides a new application of G15 in treating white matter injury and long-term neurological dysfunction by promoting cerebrovascular generation.

Provided herein are compounds, methods, and pharmaceutical compositions for reducing the amount or activity of TUBB4A RNA and, in some cases, the amount of TUBB4A protein in a cell or subject. Such compounds, methods, and pharmaceutical compositions are useful for ameliorating at least one symptom of a disease or condition associated with TUBB4A. Such symptoms and markers include hypomyelination, demyelination, dysphonia, myodynia, ataxia, spasm, cerebellar and / or basilar joint atrophy, hypopsia, stiffness, microcephalic deformity, focal cortical dysplasia, seizures, and kindergarten death.

Provided herein are compounds and pharmaceutical compositions thereof for inhibiting emopamil binding protein (EBP), and the use of the compounds and pharmaceutical compositions thereof in the treatment of demyelinating diseases, such as multiple sclerosis.

This invention relates to the field of biomedical technology, and provides the application of compound LY2940094 in the preparation of drugs for treating demyelinating diseases of the central nervous system. This invention verifies through modern biological techniques that compound LY2940094 can promote the differentiation of oligodendrocyte precursor cells (OPCs) into mature oligodendrocytes (OLs), thereby promoting the regeneration of myelin in the central nervous system and thus treating demyelinating diseases of the central nervous system.

The present application provides O-GlcNAc glycosidase (O-GlcNAcase, OGA) inhibitors and their applications for promoting remyelination. Specifically, by comparing the promoting effects of different types of OGA inhibitors on OPC differentiation and remyelination in the models of OPC differentiation and remyelination, the OGA inhibitors with drugability of the present application are obtained. The OGA inhibitors of the present application have wide application value in preventing and / or treating demyelination and its related diseases.

Disclosed is a protein comprising no more than three human autoantigenic proteins, wherein a first human autoantigenic protein comprises a truncated myelin oligodendrocyte glycoprotein (MOG) amino acid sequence, a second human autoantigenic protein comprises a myelin basic protein (MBP) amino acid sequence, and a third human autoantigenic protein comprises a truncated proteolipid protein (PLP) amino acid sequence. Also disclosed are related nucleic acids, pharmaceutical compositions, methods of treating a demyelinating disease, and methods of producing the proteins.

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 present invention relates to combination therapies targeting inhibitors of O-GlcNAc glycoside hydrolases and antibodies. Specifically, the invention provides application of a preparation combination of an OGA inhibitor and an antibody, and the preparation combination is used for combined treatment of demyelination and related diseases. The OGA inhibitor and the antibody are jointly applied to individuals suffering from myelin sheath injury or aplastic disorder, the promoting effect on myelin sheath regeneration and the regulating effect on immune cells can be achieved, the OGA inhibitor and the antibody have a synergistic effect, myelin sheath regeneration can be more remarkably promoted, and the OGA inhibitor and the antibody have wide application prospects in prevention and / or treatment of demyelination and related diseases.

To provide a pharmaceutical composition for treating nervous system disorders by inducing remyelination, neuroprotection, and immunomodulation.SOLUTION: A pharmaceutical composition comprising a therapeutically effective amount of a RXR agonist for use in combination with a thyroid hormone in the treatment of demyelination or neuroinflammation associated with a central nervous system disorder, the RXR agonist is 3, 7-dimethyl-6 (S), 7 (S) - methano, 7 - [1,1,4,4 - tetramethyl - 1,2,3,4 - tetrahydronaphth-7-yl] 2 (E), 4 (E) heptadienoic acid, and the RXR agonist is used in combination with a thyroid hormone to provide greater improvement in a central nervous system disorder than either the RXR agonist or the thyroid hormone alone.SELECTED DRAWING: Figure 1

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 is directed to methods for treating or preventing neuroinflammation in a subject by administering an effective amount of a single-domain antibody (sdAb) comprising SEQ ID NO:1. The method is applicable to subjects with multiple sclerosis, including secondary progressive, primary progressive, and relapsing-remitting forms. Administration may be intravenous, subcutaneous, or intrathecal, with dosage regimens including daily administration, loading and maintenance doses, or continuous infusion. The method may be initiated upon first clinical signs of central nervous system demyelination and contin- ued for at least 14 days. The sdAb may be co-administered with a pharmaceutically acceptable excipient such as mannitol, sucrose, or polysorbate 80, and optionally combined with disease-modifying therapies including interferon-β, glatiramer acetate, fingolimod, or ocrelizumab. The invention provides a targeted approach for modulating neuroinflammatory processes in neurological disorders.

The invention concerns nanovesicles of nanostructured myelin and uses thereof in the treatment of demyelinating and neurodegenerative diseases of the central (CNS) and peripheral (PNS) nervous system. Under another aspect, processes for the preparation of myelin nanovesicles having particular characteristics that make them suitable for recovery of the myelin sheath, where it is compromised, as a drug delivery system for CNS or PNS, and for immunotolerance, are described.

The present application relates to the technical field of medicine, especially relates to application of a small molecule compound LZ-09 in preparation of a medicine for treating and / or preventing multiple sclerosis. The present application adopts H2O2 damage OLN-93 cells as a nerve cell oxidative stress model, and the result shows that LZ-09 treatment significantly weakens the cell viability decrease caused by H2O2. The classic EAE model is made by using MOG35-55 to induce C57BL / 6 mice, and it is found that after LZ-09 intervention, the mouse neurological deficit symptom score is significantly reduced, and the disease progression is delayed, and spinal cord tissue HE and LFB staining find that the inflammation infiltration and demyelination are reduced. Therefore, the compound can effectively alleviate the symptoms of multiple sclerosis, can be used as a medicine for treating multiple sclerosis, and has wide development and application prospect.

One of the purposes of the present application is to provide a method and a plasmid for enhancing cell adhesion. The second purpose of the present application is to provide a cell for protein expression with enhanced adhesion. The third purpose of the present application is to provide a CBA method detection kit for autoimmune encephalitis based on the aforementioned cell. The fourth purpose of the present application is to provide a CBA method detection kit for autoimmune central nervous system demyelination disease based on the aforementioned cell.

The present disclosure discusses systems and methods for identifying biomarkers that can help with the diagnosis, prognosis, and treatment choices of patients with neurodegenerative diseases. Diffusion based magnetic resonance imaging can often fail for patients with a neurodegenerative disease because parameters fractional anisotropy, mean diffusivity, and radial diffusivity are based on simple models that can fail in the presence of neurodegeneration, such as demyelination. The present disclosure discusses systems and methods that enhance dMRI images and enable tractography to be performed on images of a damaged nervous system. The damaged tracks identified by the present system can be used as a biomarker for the assessment of patients. In some implementations, the biomarkers are converted into clinical scales that can be used to compare patients to one another or over time.

A pharmaceutical composition in the form of a transdermal patch comprising aminophylline or theophylline for use in the treatment or prevention of a hypomyelinating or a demyelinating disease or condition or a lesion of the peripheral or central nervous system where demyelination occurs. The patch may comprise a matrix layer comprising a matrix polymer, an active ingredient and a permeation enhancer.

The invention relates to the field of biological medicine, and relates to application of an interferon receptor 1 monoclonal antibody in preparation of a medicine for treating neuromyelitis optica pedigree diseases and a medicine composition. The antibody regulates immune response by inhibiting abnormal activation of an I-type interferon signal channel and down-regulating interferon stimulation gene expression, so that central nervous system inflammation and demyelination injury are relieved. The humanized IFNAR1 monoclonal antibody is independently used; the compound is combined with a B cell targeting drug to synergistically inhibit B cell activation and antibody secretion; and a bispecific antibody targeting IFNAR1 and a transferrin receptor is constructed, so that the ability of the drug to pass through the blood brain barrier is enhanced, and the concentration of the drug in the brain is improved. In-vivo and in-vitro experiments prove that the treatment scheme can effectively reduce the size of the focus of the NMOSD model and improve the neurological function, and a new precise treatment strategy is provided for AQP4 antibody positive patients.

Disclosed is a protein comprising no more than three human autoantigenic proteins, wherein a first human autoantigenic protein comprises a truncated myelin oligodendrocyte glycoprotein (MOG) amino acid sequence, a second human autoantigenic protein comprises a myelin basic protein (MBP) amino acid sequence, and a third human autoantigenic protein comprises a truncated proteolipid protein (PLP) amino acid sequence. Also disclosed are related nucleic acids, pharmaceutical compositions, methods of treating a demyelinating disease, and methods of producing the proteins.

The present invention is directed to methods for treating or preventing neuroinflammation in a subject by administering an effective amount of a single-domain antibody (sdAb) comprising SEQ ID NO:1. The method is applicable to subjects with multiple sclerosis, including secondary progressive, primary progressive, and relapsing-remitting forms. Administration may be intravenous, subcutaneous, or intrathecal, with dosage regimens including daily administration, loading and maintenance doses, or continuous infusion. The method may be initiated upon first clinical signs of central nervous system demyelination and continued for at least 14 days. The sdAb may be co-administered with a pharmaceutically acceptable excipient such as mannitol, sucrose, or polysorbate 80, and optionally combined with disease-modifying therapies including interferon-β, glatiramer acetate, fingolimod, or ocrelizumab. The invention provides a targeted approach for modulating neuroinflammatory processes in neurological disorders.

The invention discloses application of clomastine in treatment of traumatic brain injury. By constructing a rat TBI model, detecting related pathway protein change conditions in rat brain injury models of different days through WB, and detecting demyelination conditions through an electron microscope, it is proved that clomastine can improve endoplasmic reticulum stress and iron content change conditions, has a neuroprotective effect, and can be used for treating neurological diseases. And a foundation is laid for developing a new medicine for treating traumatic brain injury.

The present invention provides viral vectors for use in the treatment and prevention of diseases associated with Schwann cells by delivering polynucleotides specifically to Schwann cells and achieving Schwann cell specific expression. The present invention has particular application in treatment and prevention of Charcot-Marie-Tooth disease and other demyelinating neuropathies. The preferred vectors are adeno-associated vectors (AAV) having a Schwann cell-specific promoter from the Myelin Protein Zero (Mpz, P0) or a minimal Mpz promoter.

A system for treating a subject including a signaling device, a controller, and a stimulator. The signaling device is in communication with the input of the controller and is configured to send a signal to the controller. The stimulator is in communication with the output of the controller and is configured to stimulate an auricular branch of a vagus nerve in an ear of a subject in response to the controller receiving the signal from the signaling device.