47 results about "Remyelination" patented technology

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.

The present disclosure provides, in one aspect, compounds, compositions, and methods for reducing and / or inhibiting the activity of p38gamma. In certain embodiments, the compounds, compositions, and methods of the disclosure are useful for promoting remyelination. In certain embodiments, the compounds, compositions, and methods of the disclosure are useful for treating, preventing, and / or ameliorating one or more diseases or disorders in a subject, including but not limited to multiple sclerosis (MS), inflammatory disease, and cancer.

The subject matter described herein is directed to myelin-promoting compounds of Formula I and pharmaceutical salts thereof, methods of preparing the compounds, pharmaceutical compositions comprising the compounds, and methods of administering the compounds for the treatment of disorders, such as myelin-related disorders.

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 subject matter described herein relates to compounds of Formula A and pharmaceutically acceptable salts thereof that promote myelination, methods of making the compounds, pharmaceutical compositions comprising the compounds, and methods of administering the compounds to treat conditions, such as myelination-related conditions.

The present application relates to a kind of myelin repair auxiliary method based on neural signal modeling.The method obtains the multi-modal neural signal data such as electroencephalogram signal of individual to be rehabilitated and is preprocessed, forms preprocessed data set;Subsequently, individualized time series modeling process is executed, and the time series characteristic representation including nerve conduction velocity recovery rate, phase consistency and neural pathway integrity is generated, and individualized calibration is carried out by dynamic baseline updating mechanism.The calibrated feature representation is input to the pre-trained deep learning inference engine.The inference engine outputs myelin repair index and imbalance risk score, which is used to represent the degree of repair and predict future abnormal risk.Based on the above index, a set of intervention parameters is generated, including electrical stimulation intervention parameters, virtual rehabilitation training task difficulty and rehabilitation training rhythm, and further forming control instructions to configure virtual rehabilitation training environment and electrical stimulation execution interface, so as to realize the individualized assistance and dynamic optimization of myelin regeneration repair.

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.

The invention relates to the field of biological medicine, in particular to application of a reagent for up-regulating PEX5 expression level or improving PEX5 protein activity in preparation of a medicine for treating demyelination diseases. A lentivirus infection experiment and lysolecithin are utilized to induce a mouse demyelination model, it is found that PEX5 can promote differentiation and maturation of oligodendroglia cells and remyelination and repair of demyelination mice, and ganciclovir can promote differentiation of the oligodendroglia cells and effectively relieve demyelination diseases by promoting expression of PEX5. PEX5 can be used as a drug intervention target, and a drug for promoting expression or function of PEX5 can be used as a potential therapeutic drug for demyelination diseases.

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.

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 invention discloses application of steroid saponin of trillium tschonoskii maxim to preparation of a medicine for treating vascular dementia, and relates to the technical field of medicines. Animal experiments prove that the berberis apiacea steroid saponin can improve the spatial reference learning function of cerebral ischemia rats, improve the spatial reference memory function of the cerebral ischemia rats and enhance the long-term memory function of the cerebral ischemia rats. In addition, brain tissue damage and white matter structure damage of rats suffering from cerebral ischemia can be relieved, axonal myelin sheath microstructure reconstruction and white matter fiber reconstruction of the rats suffering from cerebral ischemia are promoted, and myelin sheath regeneration of rats suffering from vascular dementia is promoted. Network pharmacological analysis finds that the age grass total steroid saponin has a wide regulation effect on OPCs and OLs cell components and molecular functions, and further, OPCs differentiation myelin sheath inhibition related factors are regulated and controlled, and white matter myelin sheath regeneration is promoted.

The application belongs to the technical field of biological drugs, and particularly relates to a preparation method of genetically modified human bone marrow mesenchymal stem cells and application thereof in treating nervous system diseases, in particular, multiple sclerosis. The human bone marrow mesenchymal stem cells are double-modified by brain-derived neurotrophic factor (BDNF) and anti-S1PR5 nanobody, so that the activity of the human bone marrow mesenchymal stem cells is improved, the survival of neurons or oligodendrocytes is promoted, cell apoptosis is inhibited, and myelin regeneration is promoted, and the human bone marrow mesenchymal stem cells can be applied to nervous system diseases, in particular, multiple sclerosis.

The invention provides a composite active dressing for neural restoration and a preparation method and application thereof, and relates to the technical field of medical materials. The composite active dressing comprises a transdermal inner layer and a small extracellular vesicle slow-release outer layer, the transdermal inner layer is of a membrane-shaped structure and comprises a composite active component and a hydrogel matrix material, and the composite active component is selected from one or more of an anti-inflammatory component, a microcirculation improving component, an antioxidant component and a neurotrophic component; the small extracellular vesicle sustained-release outer layer is of a three-dimensional network structure and comprises small extracellular vesicles and a hydrogel matrix material. According to the invention, stable loading and layered deep delivery and release of the small extracellular vesicles are realized, the inflammatory response and microcirculation state of an injured part are improved, proliferation migration and remyelination of Schwann cells can be promoted, and axon regeneration and effective repair of nerve injury can also be promoted.

The present invention provides an NSDP1 micropeptide and its application in repairing demyelinating damage, belonging to the field of biomedicine technology. The NSDP1 polypeptide of the present invention can significantly promote the remyelination of axonal demyelinating damage, providing a new idea and method for repairing nerve demyelinating damage.

The invention provides hydrogel for repairing peripheral nerve injury as well as a preparation method and application of the hydrogel, and belongs to the field of biomedical engineering materials. The hydrogel disclosed by the invention is good in biocompatibility, has degradability, contains a double-layer cross-linked network structure, has the wetting characteristic of common hydrogel, and also has the advantages of collagen antigenicity, biodegradability, high biocompatibility, cell adaptability, tissue regeneration promotion and the like. The hydrogel can effectively promote regeneration and remyelination of nerve fibers, can promote gastrocnemius muscle recovery and promote motor function recovery, and has a good application prospect.

The subject matter described herein is directed to myelin-promoting compounds of Formula I and pharmaceutical salts thereof, methods of preparing the compounds, pharmaceutical compositions comprising the compounds, and methods of administering the compounds for the treatment of disorders, such as myelin-related disorders.

The invention discloses a substance for targeted inhibition of IRF1 gene expression and application thereof. The substance comprises nucleic acid for specifically silencing the IRF1 gene. The nucleic acid is siRNA (small interfering Ribonucleic Acid) containing the following sequence or a cloning vector for transcriptional coding of the following sequence: 5 '-TCACCAAGAACCAGGAA-3'. The siRNA is applied to preparation of drugs for regulating differentiation and apoptosis of oligodendrocyte precursor cells and drugs for promoting remyelination and repairing spinal cord injury. According to the invention, IRF1 is taken as a molecular intervention target, and IRF1 expression is reduced or inhibited, so that apoptosis of oligodendrocyte precursor cells is significantly inhibited, differentiation and maturation of the oligodendrocyte precursor cells are promoted, and the purpose of promoting myelin sheath recovery of spinal cord injury is achieved.

The present specification provides RXR agonists with both remyelination promotion and immunomodulatory activities, compositions comprising such RXR agonists, and methods using such compounds and compositions to treat a demyelination-related disorder by both promoting remyelination of neurons and modulating the immune system.

The invention relates to a myelin sheath repair auxiliary method based on neural signal modeling. According to the method, multi-modal neural signal data such as electroencephalogram signals of a to-be-recovered individual are obtained and preprocessed, and a preprocessed data set is formed; then, an individualized time sequence modeling process is executed, time sequence feature representation containing indexes such as the nerve conduction speed recovery rate, the phase consistency and the neural pathway integrity is generated, and individualized calibration is carried out through a dynamic baseline updating mechanism. The calibrated feature representation is input to a pre-trained deep learning inference engine. The inference engine outputs a myelin sheath repair index and an imbalance risk score for representing a repair degree and predicting a future abnormal risk. An intervention parameter set is generated based on the indexes, the intervention parameter set comprises electrical stimulation intervention parameters, virtual rehabilitation training task difficulty and rehabilitation training rhythms, and a control instruction is further formed to configure a virtual rehabilitation training environment and an electrical stimulation execution interface, so that personalized assistance and dynamic optimization of myelin sheath regeneration and repair are realized.

There is described a method for inducing lesion (preferably brain lesion) reduction in a patient in need thereof and / or Apparent Diffusion Coefficient (ADC) values (suggesting remyelination and reduced inflammation). The method comprises administering to the patient a therapeutically effective amount of ibogaine, ibogaine derivative, or a pharmaceutically acceptable salt and / or solvate thereof.

The invention provides walnut-derived extracellular membrane vesicles and application thereof in peripheral nerve injury repair, and relates to the technical field of biological medicines. The walnut-derived extracellular membrane vesicles (WEVs) prepared by the invention show typical vesicle form and nano-scale particle size distribution, and can still keep structural integrity after freeze-drying and long-term storage, thereby supporting the feasibility of standardized preparation and preservation of the walnut-derived extracellular membrane vesicles (WEVs). In the functional level, the WEVs can be efficiently internalized by Schwann cells (SCs) through an energy-dependent process, and the process accords with gridding protein mediated endocytosis characteristics; meanwhile, the WEVs show good biocompatibility and biological safety in vitro and in vivo. In addition, the WEVs can promote remyelination of PNI model rats, improve motion and sensory functions of the PNI model rats and relieve muscular atrophy conditions of the PNI model rats, and has an obvious treatment effect on the PNI model rats. The WEVs are expected to be used as a plant-derived nano candidate drug for treating peripheral nerve injury.

The invention relates to the technical field of medical instruments, in particular to a multi-mode nerve regeneration ultrasonic parameter optimization method and system, and the method comprises the steps: obtaining electrophysiological signals (action potential, conduction velocity and sensory / motion threshold) and metabolic signals (oxygenation index, oxygen content and hydration) of nervous tissue; judging a neural restoration stage (demyelination, axon rupture / reconnection, remyelination, outer diameter and conduction velocity stage), and determining CMAP, CV and SNAm weight parameters according to the restoration stage and the ratio of the electrophysiological signal to a normal value. By combining weight parameters and metabolic signals, dynamically optimizing ultrasonic treatment parameters (frequency, intensity, duty ratio and time) and monitoring the signals in real time, maintaining the parameters if the electrophysiological signals are recovered, and adjusting the parameters if the electrophysiological signals are reduced, so that accurate neural restoration is realized, the treatment parameters can be accurately adjusted according to individual differences of patients and a neural restoration dynamic process, and the accuracy of neural restoration is improved. The pertinence and the effectiveness of treatment are improved.

The invention provides application of glycopyrronium bromide in preparation of a medicine for treating nervous system diseases, and belongs to the technical field of biological medicines. The research finds that the novel drug glycopyrronium bromide shows a clear and excellent technical effect in the aspect of treating nervous system diseases, on one hand, the glycopyrronium bromide can inhibit the inflammatory response of glial cells by reducing infiltration of central mononuclear macrophages (MDM); on the other hand, differentiation and maturation of oligodendroglia precursor cells (OPCs) into oligodendroglia cells can be effectively promoted, and the effect of promoting myelin sheath regeneration is achieved. Multiple sclerosis is effectively improved through the dual effects of inhibiting glial cell inflammation and promoting myelin regeneration, and the medicine is a candidate medicine with great potential for treating progressive multiple sclerosis (MS).

The invention relates to the field of medicine, in particular to application of nucleic acid binding protein ZBP1 in treatment of brachial plexus root avulsion injury. Brachial plexus root avulsion and replantation operations are respectively carried out on a WT mouse and a ZBP1 gene knockout mouse, and it is confirmed that ZBP1 gene knockout can promote motor function recovery, reduce motor neuron death, increase myelin regeneration and relieve muscle atrophy. Meanwhile, the ZBP1 gene knockout can reduce the death of motor neurons and promote the recovery of motor functions. The invention aims to provide a novel treatment strategy and a medicine development and research direction for treating brachial plexus root avulsion injury.

The invention provides the application of SCD1 in preparing the medicine for treating the nerve myelin sheath injury diseases, the application reveals that SCD1 serves as a brand-new target spot for treating the sciatic nerve myelin sheath injury diseases for the first time, the target spot blank of existing targeted lipid metabolism regulation myelin sheath regeneration medicine is filled, and all-around repairing can be achieved from the molecule, form and function level; on one hand, the SCD1 can up-regulate expression of genes such as PMP22 and MPZ and promote myelin sheath synthesis from the source, and on the other hand, the SCD1 can also increase the myelin sheath thickness, reduce the number of non-marrow nerves and improve the structural integrity and stability of regenerated myelin sheaths; meanwhile, the SCD1 can prolong the dwell time of the rotating rod, accelerate the nerve conduction speed and improve dyskinesia and nerve conduction abnormity after sciatic nerve injury; besides, regulation of endogenous lipid metabolism is taken as a core mechanism, an intervention mode is safe and controllable, an experimental system is mature and repeatable, and an efficient, stable and safe new strategy is provided for clinical treatment of sciatic nerve myelin sheath injury.

The present disclosure is directed to methods of increasing remyelination in subjects in need thereof.

The application discloses application of dimethyl mercaptopropionic acid and relates to the field of medicine. Specifically, the application provides application of dimethyl mercaptopropionic acid in preparation of a medicine for treating Alzheimer's disease. In the application, the dimethyl mercaptopropionic acid can reverse changes in protein expression levels of MAG, CD9 and P2ry12 in the brain of an Alzheimer's disease model mouse, plays a role in myelin regeneration protection and nerve immune regulation, can reduce expression levels of pathological proteins A beta and tau related to Alzheimer's disease, improves spatial learning ability and spatial memory ability of the Alzheimer's disease mouse, and can be used for treating Alzheimer's disease.

The present disclosure relates to methods and compositions using RAP, a derivative of RAP, a variant of RAP, or a fragment of RAP to inhibit LRP1, a myelin debris receptor. The methods and compositions involve increasing, promoting, restoring, and / or enhancing differentiation of oligodendrocyte progenitor cells, myelin protein expression, mature oligodendrocyte marker expression, and / or myelination. The methods and compositions disclosed herein inhibit or block pathological activation of RhoA in OPCs. The methods and compositions also involve alleviating one or more symptoms of MS and treating MS, including slowing or stopping MS progression.