16 results about "Demyelinations" patented technology

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 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 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.

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.

Disclosed in the present invention is the use of an anti-Gelsolin3 antibody related to demyelinating Guillain-Barré syndrome. The use mainly comprises the following steps: collecting the serum from a GBS patient and a control individual, performing co-immunoprecipitation with a sciatic nerve protein to obtain an immune complex, separating and identifying the immune complex by using a mass spectrometer to obtain a candidate protein sequence, inserting a candidate protein coding gene into a vector, transfecting cells followed by immunofluorescence verification to determine the localization and expression of the candidate protein, constructing a candidate protein expression plasmid, expressing and purifying a recombinant protein in Escherichia coli, performing co-immunoprecipitation verification on the purified recombinant protein by using the serum from the GBS patient to determine the presence of an anti-Gelsolin3 IgG antibody, further verifying the expression of the anti-Gelsolin3 IgG antibody in the serum from the GBS patient by using a Western blot method, and verifying the binding of the serum from an anti-Gelsolin3 IgG antibody-positive patient to the sciatic nerve by using a single-fiber immunofluorescence method.

The application discloses application of an ERK5 gene as a target point in preparation of a medicine for preventing or treating cerebral white matter injury, and creatively finds that the ERK5 gene can be applied to early warning of cerebral white matter injury and preparation of a medicine under various pathological conditions. The ERK5 gene is highly expressed in microglial cells in a demyelination area of the cerebral white matter injury, and can be applied to early warning of the cerebral white matter injury. Knocking down the ERK5 gene can relieve oxidative stress and ferroptosis of microglial cells in the cerebral white matter injury and relieve mitochondrial damage, so that the ERK5 gene can be applied to preparation of a medicine for the cerebral white matter injury, and has good clinical application value.

Compositions of recombinant intravenous immunoglobulin (rIVIG) proteins and methods for purifying and using rIVIG proteins. The compositions comprise oligomeric Fc molecules that bind Fc receptors with high avidity. The rIVIG proteins are useful as immunomodulatory molecules to treat immune disorders, including autoimmune diseases, such as refractory immune thrombocytopenia, chronic inflammatory demyelinating polyneuropathy, multiple sclerosis, lupus, Graves' disease, Kawasaki disease, dermatomyositis, myasthenia gravis, Guillain-Barre syndrome, autoimmune hemolytic anemia, and other immune and inflammatory conditions. The rIVIG proteins are also useful as immunomodulatory agents for patients to reduce immune rejection of organ transplants, stem cell transplants, and bone marrow transplants. In addition, the present invention provides rIVIG proteins of non-human origin for use in veterinary immune disorders, such as canine rIVIG proteins for treating dogs with autoimmune hemolytic anemia, immune thrombocytopenic purpura, rheumatoid arthritis, or other canine immune disorders.

New uses of populations of motor neural progenitor cells are provided, including reducing reactive astrocytes, reducing glial scars, inhibiting reactive astrocyte-mediated axonal regeneration impairment, neuronal and / or oligodendrocyte death, priming for altering protein factor expression profiles in cerebrospinal fluid, promoting axonal regeneration and / or recovery, reducing demyelination, and promoting remyelination and / or increasing myelin thickness, among others.

The present invention provides a C-terminal MANF fragment with the sequence having length of 34-63 amino acids or a sequence which has at least 80 % sequence identity with the sequence, wherein said fragment is a cell membrane penetrating peptide, for use in the treatment of a demyelinating disease such as multiple sclerosis, wherein said fragment is preferably administered subcutaneously.

This invention belongs to the field of biomedical technology and discloses the application of the SSRP1 gene as a target in the preparation of drugs for the prevention or treatment of NMOSD. These drugs contain components that target and interfere with the SSRP1 gene or its expression. This invention creatively discovers the application of the SSRP1 gene as a target in the preparation of drugs for the prevention or treatment of NMOSD. Knockdown of SSRP1 can alleviate motor balance impairment in NMOSD, improve the severity of demyelination damage in NMOSD, improve the myelin regeneration microenvironment in NMOSD, alleviate microglial activation caused by NMOSD, alleviate microglial-mediated neuroinflammation in NMOSD, and alleviate microglial ferroptosis in NMOSD. Therefore, it can be applied to the preparation of drugs for the treatment of NMOSD and has good clinical application value.

The application of β-asarone ether in the preparation of drugs for promoting myelin regeneration, for improving neurological dysfunction in organisms with myelin injury, inhibiting inflammatory demyelination in the central nervous system, and enhancing memory and cognitive function.

This application discloses the use of neuroprotective agent D1 (NPD1) in the preparation of drugs to relieve / treat chronic pruritus, relating to the field of biomedical technology. This invention provides NPD1 that can reverse spinal cord demyelination and relieve chronic pruritus. NPD1 can be used to relieve and / or treat chronic dermatitis pruritus, particularly showing excellent inhibitory effects against allergic contact dermatitis. The NPD1 can be developed into conventional lipid nanoparticles (LNPs) or other similar lipid nanoparticle drug formulations for drug delivery, possessing significant potential application value for relieving itching. The NPD1 developed in this invention can directly relieve pruritus abnormalities caused by dorsal horn demyelination of the mouse spinal cord, fundamentally inhibiting the occurrence of pruritus abnormalities in chronic dermatitis, solving the clinical problem of chronic pruritus that plagues patients with chronic dermatitis, and providing a new and effective solution for the clinical treatment of chronic dermatitis, especially pruritus in allergic contact dermatitis.