226 results about "Demyelinations" patented technology

The present invention relates to methods of treating Chronic Inflammatory Demyelinating Polyneuropathy (CIDP) using an antagonist of human neonatal Fc receptor (FcRn), which in certain embodiments is efgartigimod.

Systems, devices, and methods for using vagus nerve stimulation to treat demyelination disorders and / or disorder of the blood brain barrier are described. The vagus nerve stimulation therapy described herein is configured to reduce or prevent demyelination and / or promote remyelination to treat various disorders related to demyelination, such as multiple sclerosis. A low duty cycle stimulation protocol with a relatively short on-time and a relatively long off-time can be used.

Method for reversing demyelination in a patient having a demyelinating disorder may include detecting one or more biomarkers for demyelination from the patient, receiving, in an implanted vagus nerve stimulator, a command to apply a remyelinating stimulation to the patient based on a level of the detected one or more biomarkers for demyelination; and applying electrical stimulation to the patient's vagus nerve from the implanted vagus nerve stimulator to reverse demyelination and increase remyelination of the patient's nerves. The electrical stimulation may be adjusted based on the level of the detected one or more biomarkers.

Systems, devices, and methods for using vagus nerve stimulation to treat demyelination disorders and / or disorder of the blood brain barrier are described. The vagus nerve stimulation therapy described herein is configured to reduce or prevent demyelination and / or promote remyelination to treat various disorders related to demyelination, such as multiple sclerosis. A low duty cycle stimulation protocol with a relatively short on-time and a relatively long off-time can be used.

The invention belongs to the technical field of exosome modification, and particularly relates to an exosome modification method for connecting a target protein to the surface of an exosome by utilizing NHS-PEG-NHS to achieve a targeting or treatment effect, and application of the exosome modification method in targeted central nervous system demyelination disease treatment. In particular to a technology for modifying an exosome to enable the exosome to have targeting property and a preparation method of the exosome. NHS-PEG-NHS is used as a connecting substance, and protein, polypeptide and substances with primary amine groups on the surface can be connected to the surface of an exosome membrane. The modified exosome can load drugs and can be accurately delivered to tissues expressing specific proteins or polypeptides through oral administration, so that the bioavailability and the treatment effect of the drugs are remarkably improved. Taking the NG2 antibody modified cow milk exosome as an example, the NG2 antibody is connected to the surface of the cow milk exosome to target the central demyelination focus area, so that the effective therapeutic dose of the drug in the central focus area is achieved through oral delivery.

This application relates generally to the field of Bone Morphogenetic Protein (BMP) antagonists (soluble ALK6 fusion proteins), compositions thereof, and methods for use in treating neurodegenerative diseases and / or demyelinating diseases.

The invention relates to an antibody detection kit for detecting chronic inflammatory demyelinating multiple nerve root neuropathy and a preparation method of the antibody detection kit. The antibody detection kit for detecting the chronic inflammatory demyelinating multiple nerve root neuropathy comprises an IgG antibody detection strip, an IgM antibody detection strip, a working solution and an auxiliary agent. The antibody detection kit disclosed by the invention can be used for simultaneously detecting nine autoantibodies related to the chronic inflammatory demyelinating multiple nerve root neuropathy, wherein the nine autoantibodies comprise NF155, NF186, CNTN1, CNTN2, CASPR1, CASPR2, GLIOMEDIN, NRCAM and MAG. The design of simultaneous detection of multiple antigens greatly improves the comprehensiveness of detection, so that multiple possible pathogenic factors can be covered in single detection, and the problem of missed diagnosis caused by single antibody detection is avoided.

An EAE mouse model proves that the kaempferol and the ephedra, radix aconiti carmichaeli and herba asari particles can obviously save the myelin sheath damage of a mouse. Meanwhile, through serum metabolome analysis and metabolome and transcriptome analysis, the binding force of kaempferol and MMP3 is predicted, and through an EAE mouse model, it is proved that kaempferol can reduce expression of MMP3 through binding with MMP3, and IL-17 and demyelination are inhibited, so that the disease progression of EAE is delayed. Therefore, the invention proves that the kaempferol and the ephedra, monkshood and asarum granules can be used for treating and / or relieving the multiple sclerosis (MS), and the invention provides a new way for the treatment of the multiple sclerosis (MS).

The invention relates to the technical field of biological medicine, and particularly discloses application of Si-Ikzf1 in preparation of products for inflammation treatment and neuroprotection, the Si-Ikzf1 provided in the scheme of the invention reduces formation of cell eschar by promoting microglial cell MResident subtype to be generated into MPtn subtype instead of MIkzf1, and improves post-ICH neurological functions by regulating Ikzf1-SIRT1 and downstream signal pathways thereof. The scheme of the invention reveals high expression of inflammatory bodies and scorch symptom related proteins in MIkzf1 subtype microglial cells, and Si-Ikzf1 can promote the conversion of MResident in ICH rats to MPtn instead of MIkzf1, and the MPtn represents an anti-inflammatory effect of promoting nerve remodeling, and the Si-Ikzf1 is capable of promoting the conversion of MResident in ICH rats to MPtn in ICH rats to MPtn in ICH rats to MPtn in ICH rats to MPtn in ICH rats. It is revealed that Si-Ikzf1 hinders MIkzf1 inflammation, scorch symptom and cell apoptosis, so that cognitive behavior and demyelination injury are improved; moreover, the scheme of the invention proves that the Si-Ikzf1 can reverse the reduction of SIRT1 expression in BV-2 cells and ICH rat brains after inflammation stimulation, and promote the up-regulation of Ptn in MPtn.

The use of α-ketoglutaric acid in the preparation of a drug for preventing and treating demyelination-related diseases. The α-ketoglutaric acid or a derivative thereof is used for preventing and / or treating myelin sheath defects in demyelination-related diseases, such as demyelinating diseases, amyotrophic lateral sclerosis, Huntington's disease, hypomyelinating leukodystrophy, Alzheimer's disease, Parkinson's syndrome and diabetes-related visual impairment, and can promote myelin sheath generation, regeneration or repair, and improve the immune microenvironment in the lesion area.

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.

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 alpha 1-antitrypsin (AAT) proteins, variants, isoforms and / or fragments thereof and / or corresponding nucleic acid sequences thereof for use in the treatment of diseases or disorders of the nervous system, such as chronic inflammatory demyelinating polyneuropathy. The invention also relates to combinations with IgG antibodies, such as immunoglobulin therapy, for use in these diseases or disorders.

To provide a biomarker, a diagnostic kit, and a method of assisting in diagnosis for the specific diagnosis of a group having specific disease state physiology in acute and chronic inflammatory demyelinating peripheral neuropathy with unknown autoantibody.SOLUTION: There are provided a biomarker, a diagnostic kit containing the same, and a method of assisting in diagnosis for using the same for diagnosis of inflammatory demyelinating polyneuropathy, including anti-LGI4 antibodies, or for determination of the efficacy of treatment, or the inflammatory demyelinating polyneuropathy being an autoimmune neuropathy.SELECTED DRAWING: None

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 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.

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.

The present invention belongs to the field of biomedical technology, and particularly relates to the use of dendritic cells in the prevention and / or treatment of demyelinating diseases. The expression level of Talin1 protein in the dendritic cells is reduced or not expressed. Loading the dendritic cells with myelin peptides can safely and effectively alleviate immune inflammation and nerve damage, and thus is expected to develop into a new therapy for the prevention and / or treatment of demyelinating diseases.

The invention features compositions and methods for treating diseases or disorders associated with undesirable neuronal excitability (e.g., de-myelinating disease, neurodegenerative disease, such as Parkinson's disease or Huntington's disease; or chronic pain, or epilepsy).

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.

Disclosed herein are methods and compositions for treating a demyelinating disease, such as multiple sclerosis, by administering to a subject suffering from the disease at least one Retinoid X receptor gamma (RXRy) agonist and at least one member selected from a Liver X Receptor (LXR) antagonist, CYP51 inhibitor, TM7SF2 inhibitor, EBP inhibitor, and combinations thereof.

The present invention provides the use of the small molecule compound 2-D08 in the preparation of a drug for treating or preventing demyelinating diseases. As a small molecule compound, 2-D08 has a small molecular weight and is easily permeable through the blood-brain barrier to exert central pharmacodynamic effects. Moreover, the chemical synthesis method of 2-D08 is also very mature, which is conducive to reducing the preparation cost of drugs for treating demyelinating diseases, thereby alleviating the medical expenses of patients to a certain extent. 2-D08 can promote the regeneration of myelin sheaths of spinal cord axons, significantly improve the motor ability and nerve function recovery of mice, and is expected to become a disease-modifying treatment drug targeting the origin of brain damage in MS patients, with brain permeability and ion channel selectivity, and has very broad application prospects.

Provided herein are compounds and compositions useful in increasing PPARδ activity. The compounds and compositions provided herein are useful for the treatment of PPARδ related diseases (e.g., muscular diseases, vascular disease, demyelinating disease, and metabolic diseases).

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.

To provide a drug having positive effects in subjects suffering from neurological diseases, including neurodegenerative diseases, demyelinating diseases, neuro ischemic diseases and neuromuscular diseases.SOLUTION: Dextran sulfate, or a pharmaceutically acceptable derivative thereof, is used to induce differentiation of glial cells and neurons.SELECTED DRAWING: Figure 12

Described herein are compositions for treating human patients exhibiting hyperactivity of PAD enzymes, hypercitrullination and / or a neurodegenerative disease exhibiting a demyelinating condition, or treating multiple sclerosis in human patients in need thereof. Also described herein are methods of treating a human patient exhibiting hyperactivity of PAD enzymes, hypercitrullination and / or a neurodegenerative disease exhibiting a demyelinating condition, or multiple sclerosis in human patients in need thereof, including orally administering to the patient once or twice daily a compound of Formula (I) or a pharmaceutically acceptable salt thereof.

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.