12 results about "Glial scar" 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.

The invention relates to a spinal cord injury repair method based on four-dimensional multifunctional hydrogel, which comprises the following steps: firstly, encapsulating NT-3 in PLGA (poly (lactic-co-glycolic acid)) microspheres through a microsphere technology, and integrating HCT (Hydroxycycline Computed Tomography) into SilMA hydrogel, so as to construct four-dimensional multifunctional hydrogel 4DMSH with time specificity; the hydrogel shows a remarkable anti-inflammatory effect in an in-vivo experiment, can effectively inhibit the inflammatory reaction at the early stage of spinal cord injury, promotes eNSCs to differentiate into neurons by improving a microenvironment and inhibits formation of glial scars, so that the nerve repair efficiency is improved; the four-dimensional multifunctional hydrogel has time specificity and can create an anti-inflammatory and neuroactive microenvironment, so that effective spinal cord injury repair and nerve regeneration are realized; the hydrogel can be widely applied to SCI treatment, and a brand new strategy is provided for repairing nervous system injury.

The invention discloses an external field generator, a probe based on external field driving and a neural electrode system. Wherein the neural electrode system comprises an external field generator and a probe which are in signal connection; the probe is used for being fixed in a designated brain area and collecting action potentials of neurons in the brain, and the probe is provided with a composite coating containing an external field response material and a conductive material. The external field generator is used for driving the external field response material in the composite coating to drive the conductive material to perform gradient migration along the short axis of the scar so as to form a continuous conductive micro-channel. The external field response conductive material is used between the glial cells to construct the conductive micro-channel, so that the insulated glial scar is converted into the artificial neural pathway, the total impedance of an electrode-tissue interface is reduced by a plurality of orders of magnitude, the fidelity of electroencephalogram signals is remarkably improved, and the service life of the electrode is prolonged.

A spinal cord injury repair method based on biphase fibroin and methacryloyl hydrogel comprises the following steps: firstly, encapsulating NT-3 and NSCs in PLGA microspheres through a microsphere technology, and integrating Ang-(1-7) into SilMA hydrogel, so as to construct the biphase SilMA multifunctional hydrogel (DPSH) with time-specific drug controlled release. The hydrogel shows a remarkable anti-inflammatory effect in an in-vivo experiment, can effectively inhibit the inflammatory reaction at the early stage of spinal cord injury, promotes NSCs to be differentiated into neurons by improving a microenvironment and inhibits formation of glial scars, so that the nerve repair efficiency is improved.

Provided herein are compositions, systems, kits, and methods for treating glial scarring caused by injury to a central nervous system (CNS) site by administering a CSPG reduction peptide (CRP), or a nucleic acid sequence encoding the CRP. In particular embodiments, CNS site is the result of a stroke in a subject (e.g., human subject that has had a stroke). In certain embodiments, the CRP is composed of a cell membrane penetrating domain, a lysosome targeting domain, and a chondroitin sulfate proteoglycan (CSPG) binding domain.

This invention discloses an electromagnetic modulation method for improving the formation of glial scars around implanted electrodes. The method selects at least two electrode channels in an implanted brain-computer interface electrode array as stimulation channels and connects them to an external stimulation driving circuit. By outputting a charge-balanced low-frequency pulse stimulation current, it implements staged modulation of the local tissue around the electrodes at different stages after implantation. Simultaneously, it continuously monitors the electrode-tissue interface impedance and / or the signal-to-noise ratio of neural signals, and performs closed-loop switching between different stimulation parameters based on the monitoring results. This method is drug-free and can utilize bipolar or tripolar current-guided stimulation configurations to regulate the spatial distribution of the local electric field. Combined with the accompanying near-field electromagnetic effect, it provides electromagnetic parameter-dependent long-term modulation of the inflammatory response of microglia and astrocytes at the implantation interface, thereby improving the long-term electrical stability of the implantation interface and extending the lifespan of the implanted electrodes.

The application discloses a kind of fusion polypeptide TGNL and its modified neural stem cell in the application of spinal cord injury repair.The fusion polypeptide TGNL is composed of TAT penetration domain, GSTP targeting domain, NICDi inhibiting domain, MMP-2 activation domain and flexible Linker connecting them, and full-length amino acid sequence is shown as SEQ ID NO.1.The application also provides the preparation method of the polypeptide, neural stem cell (hNSCs-TGNL) expressing the polypeptide and its construction method.Experiments show that the fusion polypeptide TGNL can efficiently penetrate nerve cells, specifically target glial scar, be selectively activated by MMP-2, and promote neural stem cell differentiation into neuron by inhibiting Notch signal;hNSCs-TGNL has high survival rate and strong penetration ability in in-vitro glial scar model, can significantly promote motor function recovery, reduce injury volume, increase axon density and reduce glial scar in rat spinal cord contusion model.The application provides a new candidate drug and cell treatment strategy for clinical treatment of spinal cord injury, and has significant clinical application value.

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 disclosure relates to the use of, and to methods of using, DHODH inhibitor compounds, pharmaceutically acceptable salts thereof, and pharmaceutical compositions including a DHODH inhibitor compound for the treatment of ocular diseases. The ocular diseases include, but are not limited to, proliferative vitreoretinopathy, cystoid macular edema, central serous retinopathy, diabetic retinopathy, endophthalmitis, epiretinal membrane, and toxoplasmosis. The present disclosure also relates to the use of, and to methods of using, DHODH inhibitor compounds, pharmaceutically acceptable salts thereof, and pharmaceutical compositions including a DHODH inhibitor compound to inhibit glial scar formation or reduce glial scar length.

The present disclosure relates to the use of, and to methods of using, DHODH inhibitor compounds, pharmaceutically acceptable salts thereof, and pharmaceutical compositions including a DHODH inhibitor compound for the treatment of ocular diseases. The ocular diseases include, but are not limited to, proliferative vitreoretinopathy, cystoid macular edema, central serous retinopathy, diabetic retinopathy, endophthalmitis, epiretinal membrane, and toxoplasmosis. The present disclosure also relates to the use of, and to methods of using, DHODH inhibitor compounds, pharmaceutically acceptable salts thereof, and pharmaceutical compositions including a DHODH inhibitor compound to inhibit glial scar formation or reduce glial scar length.

The invention relates to the field of medical instruments, and provides a composite immune scaffold for promoting spinal cord repair after injury and application, the composite immune scaffold is formed by printing through a three-dimensional printing technology, the composite immune scaffold comprises at least two matrix layers and at least one support layer, the support layer is located between the at least two matrix layers, and the matrix layers are arranged on the support layer. IRF4 proteins are distributed inside and / or on the surfaces of the supporting layer and the matrix layer. When the composite immune scaffold is delivered to a spinal cord injury part, the matrix layer and the supporting layer can fill the injury area to maintain the spinal cord contour structure, and meanwhile, the matrix layer and the supporting layer can well bear IRF4 protein, so that IRF4 is enriched at the spinal cord injury part, and the IRF4 protein can be continuously released at the spinal cord injury part; the compound can inhibit the polarization of M1 type macrophages in an immune microenvironment and promote the polarization of M2 type macrophages, is beneficial to the formation of a microenvironment for nerve regeneration, promotes the regeneration of neurons and axons, inhibits the formation of glial scars, and promotes the repair after spinal cord injury.

Provided herein are compositions, systems, kits, and methods for treating glial scarring caused by injury to a central nervous system (CNS) site by administering a CSPG reduction peptide (CRP), or a nucleic acid sequence encoding the CRP. In particular embodiments, CNS site is the result of a stroke in a subject (e.g., human subject that has had a stroke). In certain embodiments, the CRP is composed of a cell membrane penetrating domain, a lysosome targeting domain, and a chondroitin sulfate proteoglycan (CSPG) binding domain.