168 results about "Microglia" patented technology

The present invention provides an isolated antibody that binds a fibrin or fibrinogen γC domain. In various aspects, the antibody inhibits microglial adhesion to the fibrin or fibrinogen γC domain, inhibits Mac-1 binding to the fibrin or fibrinogen γC domain, and/or suppresses clinical symptoms of Experimental Autoimmune Encephalomyelitis (EAE). Various methods of using the antibodies, pharmaceutical compositions, kits, vectors, cells comprising the vectors, and antibody generating methods are provided.

The invention relates to a biological microglia comprising at least two pores having a size adopted to allow cells, cell aggregates, tissue or other biological material to pass through said pores, and one or several slicing beams separating said pores from each other, wherein biological material is split/sliced/cleaved into at least two parts when passing said microgrid, a slicing device, an apparatus comprising said slicing device as well as the use of said microgrid, slicing device and apparatus.

A neuronal cell death inhibitor comprising a compound having an inhibitory activity on the production and/or release of glutamic acid in a microglia; by inhibiting the production and/or release in a microglia, neurite bead-like degeneration or neuronal cell death can be inhibited.

A method is provided for inducing and enhancing neurogenesis and/or oligodendrogenesis from endogenous as well as from exogenously administered stem cells, which comprises administering to an individual in need a neuroprotective agent such as a nervous system (NS)-specific antigen, a peptide derived therefrom, T cells activated therewith, poly-YE, microglia activated by IFN-γ and/or IL-4 and combinations thereof. The method includes stem cell therapy in combination with the neuroprotective agent.

Filamentous bacteriophage which does not display an antibody or a non-filamentous bacteriophage antigen on its surface is used to inhibit or treat brain inflammation associated with amyloid deposits and/or involving activated microglia, to inhibit the formation of amyloid deposits, and to disaggregate pre-formed amyloid deposits.

The present invention relates to the usage of wilfordii chlorine lactonic alcohol T4 for curing neural immune inflammatory diseases and provides a new usage of the wilfordii chlorine lactonic alcohol T4 for curing neural immune inflammatory diseases caused by the neural toxicity of microglia-mediated ABeta1-42 and LPS. The traditional medicine monomer of the wilfordii chlorine lactonic alcohol T4 has the following functions: obviously reducing the toxic damages of the oligmeric ABeta1-42 and LPS-induced gel-inflammation reaction on nerve cells, so as to protect the survival of nerve cells; inhibiting the level of inflammation medium produced by the oligmeric ABeta1-42 and the LPS-induced microglia cells; inhibiting the increase of iNOS and COX-2 expression of the oligmeric ABeta1-42 and the LPS-induced microglia cells; inhibiting the activation of NF-KappaB and JNK signal access of the oligmeric ABeta1-42 and the LPS-induced microglia cells. Therefore, the present invention provides direct powerful experimental evidence and theoretical basis for the application of the wilfordii chlorine lactonic alcohol T4 in neural immune inflammatory diseases, especially prevention and treatment of Alzheimer disease, thus having strong scientificity and creativity, as well as high development and application value.

The invention discloses an application of gastrodin to preparing medicaments for preventing and treating Alzheimer's disease. Alzheimer's disease (AD) is a neurodegenerative disease, and pathological characteristics comprise neuro fibrillary tangles formed in cells, hyperplasia of reactive microglia and glial cell, and the like, wherein the extracellular deposition of amyloid A beta is the main pathogenetic reason of AD. An AD small mouse taking a gastrodin-containing fodder is substantially improved in spatial-memory learning ability, substantially reduced in A beta level in brain and serum, and substantially reduced in amyloid plaques and microglia in brain tissue, and thus it is indicated that gastrodin is capable of preventing A beta deposition and decreasing active components causing AD mouse brain gastrodin.

The present invention describes a method for the in vitro diagnosis, prognosis and/or treatment monitoring of neurodegenerative, neurological and inflammation-based diseases, wherein the method comprises the steps: a) isolating microglial microvesicles (MVs) from biological fluids obtained from an individual; b) collecting the microRNA (miRNA) contained into said MVs; c) determining the expression profile of a predetermined set of miRNA; d) comparing said expression profile to one or several reference expression profiles, wherein the comparison of said determined expression profile to said one or several reference expression profiles allows for the diagnosis, prognosis and/or treatment monitoring of the disease.

The invention relates to pharmaceutical compositions, kits, methods, and uses for the treatment of amyotrophic lateral sclerosis. In particular, the invention relates to compositions, kits, methods, and uses for the treatment of amyotrophic lateral sclerosis by inhibiting NF-κB in microglia or macrophages and by inhibiting motor neuron death. The invention further relates to compositions, kits, methods, and uses for the treatment of amyotrophic lateral sclerosis by inhibiting NF-κB in microglia in combination with inhibiting SOD-1 in astrocytes. The invention also relates to a method for inhibiting the expression or the activity of NF-κB in microglia or macrophages to inhibit motor neuron death, alone or in combination with inhibiting SOD-1 expression in astrocytes.

The invention provides a functional polypeptide. The functional polypeptide includes a polypeptide fragment I identifying and blocking amyloid protein A beta aggregation and a polypeptide fragment IIwhich is a mimic peptide of an apoE receptor binding region, and the polypeptide fragment I and the polypeptide fragment II are linked through a linker peptide or directly linked. The polypeptide caninhibit amyloid protein A beta aggregation, inhibit the of A beta, accelerate removal of A beta through microglia, and the functional polypeptide can be used for preparing drugs for treating the Alzheimer disease.

The invention belongs to the field of tumour basic research, and relates to a method used separating and purifying microglia cells from glioma specimens. The method comprises following steps: a cell suspension is prepared from tumour tissues via mechanical method combined with enzymatic digestion method; the cell suspension is subjected to density gradient centrifugation so as to obtain the microglia cells of CD11B+ with a relatively high purity via enrichment and selection; and the microglia cells with a relatively high purity are obtained via further separation using CD11B+ magnetic beads. Wherein, Percoll separating medium is composed of 70% of Percoll, 30% of Percoll, and HBSS. The purity of the microglia cells obtained via percoll density gradient centrifugation enrichment can be more than 95%, and it is confirmed by immunofluorescence assay and phagocytosis assay that functions of the microglia cells are excellent. The method is simple and convenient for operation, is low in cost, is stable in quality, and is capable of providing basis for further research on immunologic functions microglia cells in brain glioma and effects of microglia cells in immune escape of tumour.

The invention discloses diagnosis and treatment methods of Alzheimer disease and a corresponding kit. Specifically, an expression level of TREM1 (Triggering Receptor Expressedon Myeloid 1) proteins directly influences a clearing-up capability of microglial cells on beta amyloid proteins, so that the beta amyloid proteins cannot be normally cleaned; and the TREM1 proteins can be used as diagnosis and treatment target spots of the Alzheimer disease.

Methods are provided for protecting an individual from adverse long-term effects of neuroinflammation. Inflammatory blockade maintains neurogenesis capability after cranial irradiation by reducing the negative effects of activated microglia on neural precursor cells. These findings have broad implications for a variety of diseases of cognition, involving neuroinflammation and precursor cell dysfunction.

The invention discloses a gene-vector composition of targeted microglia. The gene-vector composition is formed by combining a CX3CR1shRNA (Ribose Nucleic Acid) interference vector and a gene vector through an electrostatic interaction, wherein the gene vector is conjugate of H9 polypeptide and chitosan; the composition can be successfully targeted to a specific CX3CR1 acceptor molecule on the surface of the microglia under the guiding action of the H9 polypeptide; and while the H9 polypeptide exerts the antagonism for a CX3CR1 acceptor, the CX3CR1shRNA interference vector can be efficiently transfected into the microglia to intervene the expression of the CX3CR, inhibit the activation of the microgli and further inhibit the generation or deterioration of microglia-medicated nervous system diseases. The invention also discloses a preparation method of the gene-vector composition. The preparation method is simple and convenient to operate; the obtained gene-vector composition is nanoparticles with uniformity in size so as to bring convenience to uptake of cells; the gene-vector composition disclosed by the invention can be used for preparing a microglia activator inhibitor and has favorable development and application prospect in the field of treatment on the microglia-medicated nervous system diseases.

Methods of suppressing the activation of microglial cells in the Central Nervous System (CNS), methods of ameliorating or treating the neurological effects of cerebral ischemia or cerebral inflammation, and methods of combating specific diseases that affect the CNS by administering a compound that binds to microglial receptors and prevents or reduces microglial activation are described. ApoE receptor binding peptides that may be used in the methods of the invention are also described, as are methods of using such peptides to treat peripheral inflammatory conditions such as sepsis. Also described are methods of screening compounds for the ability to suppress or reduce microglial activation.

The invention discloses a pharmaceutical composition which is specially the pharmaceutical composition for treating ischemic cerebral stroke. The pharmaceutical composition is based on total weight ofthe composition and comprises 18.1%-50.9% of lactone constituents, 48.8%-81.8% of flavonoid constituents and 0.07%-6.83% of organic acid constituents. The pharmaceutical composition including the lactone constituents, the flavonoid constituents and the organic acid constituents and application thereof in the treatment of the ischemic cerebral stroke are not reported in the prior art. The pharmaceutical composition of the invention can effectively reduce cerebral infarction area of a mouse of a cerebral ischemia reperfusion model and reduce a neurological function score of the mouse, can significantly improve the activity of neuron cells of an oxygen-glucose deprivation/hypoxia-reoxygenation neuron cell damage model, has a substantial protection effect on an inflammation of LPS induction microglia, is safe and effective, and can be prepared as a drug for preventing or treating the ischemic cerebral stroke.

The invention discloses the application of thunder god vine monomeric compound in improving the efficiency of the adeno-associated virus vector mediated gene expression, and also discloses the application of the thunder god vine monomeric compound in the adjuvant therapy for neurodegenerative diseases. The thunder god vine monomeric compound, in particular to Triptolide, can remarkably improve the transduction efficiency of 2-typed recombinant adeno-associated virus on a plurality of nerve cell systems, primary nerve cells and midbrain nervous tissues of rats. In addition, the thunder god vine monomeric compound can inhibit the activation of microglia, reduce the production of proinflammatory cytokine, increase the generation of neurotrophic factors and have protection effect on dopaminergic neuron and can be used for adjuvant therapy for neurodegenerative diseases. The invention effectively overcomes the bottleneck problem in the gene treatment of AAV-mediated neuropathy, fully combines the protection effect of the thunder god vine monomeric compound on nerve cells with the assistant synergy effect on virus vector and reduces the potential immune side effect and application cost.

The invention discloses application of cobra neurotoxin monomer molecules in treatment of senile dementia. The senile dementia, also known as Alzheimer disease, is a senile disease with progressive memory disorder, obstacle of judgment and reasoning ability as well as dyskinesia as main clinical features. Evidence shows that strong focal inflammatory responses exist in the brains of the patients with the senile dementia, and activated microglia and astrocytes exist near senile plaques; and the activated microglia and astrocytes can express a plurality of inflammatory cytokines, including interleukin-1[beta] (IL-1[beta]), tumor necrosisfactor-alpha (TNF-alpha) and the like. Therefore, experts suggest that neurodegeneration may be caused by inappropriate activation of immune and inflammatoryreactions in the brain; and super-strong immune reactions can attack nerve tissue "in the wrong direction", thereby causing neuron damage and death. In order to solve the problems, the invention discloses a group of cobra neurotoxin monomer molecules which can inhibit increase of contents of related inflammatory factors, namely the IL-1[beta]) and the TNF-alpha, in the hippocampus of rats with the senile dementia, as well as significantly shorten escape latency of the rats with the senile dementia after treatment in Morris water maze experiment.

An active agent that causes an increase in the number of disease-associated microglia (DAM) for use in treating a neurodegenerative disease is provided.

The invention relates to a medicament for treating neurodegenerative diseases and particularly relates to an application of chitosan oligosaccharide in preparation of medicaments for preventing and/or treating neurodegenerative diseases, i.e., the chitosan oligosaccharide can be further applied to the medicaments for preventing and/or treating the neurodegenerative diseases. According to the medicament and the application thereof, with lipopolysaccharide (LPS) as an inducing factor and mouse microglia as a research object, a result shows that the chitosan oligosaccharide can remarkably restrict the expression of the activated microglia iNOS (Inducible Nitric Oxide Synthase) in mRNA (Messenger Ribonucleic Acid) and protein level, can restrict the generation of activated microglia NO (Nitric Oxide), can effectively restrict the generation of activated microglia ROS (Reactive Oxygen Species), can effectively restrict the activation of an MAPK (Mitogen Activated Protein Kinase) signal channel caused by LPS, and can effectively restrict the activation of transcription factor NF-kB (Nuclear Factor-Kappa B) and AP-1 (Activator Protein-1).

The invention discloses novel medicinal application of baicalein, in particular to application of the baicalein to the preparation of medicament for treating demyelinative diseases of central nervous system. The baicalein shows favorable treatment functions on an experimental allergic cerebrospinal meningitis model of a mouse and the treatment functions are achieved by inhibiting microglia 12/15 lipoxygenase in the central nervous system and adjusting the expression condition of a group of molecules with nerve protecting functions, such as FIZZ1 (foundininflammatoryzone1), MRC1 (mannose receptor, C type 1) and Arg1 (arginase 1) on the mRNA (messenger ribonucleic acid) level, thereby inducing high-level M2 type microglia in the central nervous system. The M2 type microglia has the function of CNS (central nervous system) neuroendocrine nutrilit and can promote the repair of medullary sheath, thereby relieving the progress of disease conditions.

A method of treating a subject suffering from a neurodegenerative disease by modulating microglial activation with a therapeutically effective amount of a cholinergic agonist and a cholinesterase inhibitor. In one embodiment of the invention, the cholinergic agonist is nicotine and the cholinesterase is galantamine (a relatively weak acetylcholinesterase inhibitor and a potent allosteric potentiating ligand of nAChRs)