46 results about "Motor neuron" patented technology

The invention is directed to a method of administering motoneuronotrophic factors for promoting the survival, growth, proliferation, or maintenance of mammalian neurons. The method is useful for promoting the survival, growth, proliferation, regeneration, or maintenance of mammalian neurons, promoting axonal regeneration, for inhibiting the effects of hereditary motoneuron disease, for minimizing or inhibiting the effects of scar tissue formation, and for accelerating wound healing while concomitantly minimizing or inhibiting the effects of scar tissue and keloid formation.

A method for forming neuromuscular junctions includes forming functional neuromuscular junctions between motoneurons and muscle cells by co-culturing one or more human motoneurons and one or more rat muscle cells in a substantially serum-free medium. A synthetic mammalian neuromuscular junction includes a human motoneuron functionally linked to a rat muscle cell in a substantially serum-free medium. An artificial substrate may be used to support the one or more neuromuscular junctions.

A method for forming neuromuscular junctions includes forming functional neuromuscular junctions between motoneurons and muscle cells by co-culturing one or more human motoneurons and one or more human muscle cells in a substantially serum-free medium. A synthetic mammalian neuromuscular junction includes a human motoneuron functionally linked to a human muscle cell in a substantially serum-free medium. An artificial substrate may be used to support the one or more neuromuscular junctions.

A method for determining the level of survival motor neuron (SMN) protein in a whole blood or cerebral spinal fluid (CSF) sample, for example, a whole blood lysate sample or a CSF sample, including obtaining a whole blood or cerebral spinal fluid (CSF) sample from the subject and conducting an electrochemiluminescence immunoassay to determine the level of SMN in the whole blood or cerebral spinal fluid (CSF) sample.

The invention provides a method for preparing motoneuron-like cells derived from adipose stem cells. The method comprises the following steps: treating 3-6 generations of high-purity adipose stem cells by using a motoneuron-like cell inducer to obtain motoneuron-like cells; and treating the adipose stem cells by using the motoneuron-like cell inducer, and then treating continuously by using neurotrophic factors, thereby obtaining more mature motoneuron-like cells. By adopting the method provided by the invention, the more mature motoneuron-like cells derived from the adipose stem cells can be obtained in an extremely short time, and the obtained motoneuron-like cells can be used for preventing or treating motoneuron injuries and spinal cord injuries; and the pre-induced motoneuron-like cells obtained by the method provided by the invention can be better used for preventing and treating the motoneuron injuries and spinal cord injuries.

The present invention provides a method of inducing myelination of isolated motoneurons by preparing a non-biological substrate having thereon a covalently attached monolayer of DETA; depositing isolated motoneurons on the substrate in a defined serum-free medium; plating isolated Schwann cells cultured in the defined serum-free medium onto the motoneurons, thereby initiating a co-culture; and passaging the co-culture as necessary into fresh, defined serum-free medium supplemented with L-ascorbic acid at least until the motoneurons form Nodes of Ranvier indicative of myelination. The invention also includes a method of testing for new drugs effective in demyelinating diseases. Additionally, cellular products provided by the invention include an isolated motoneurons myelinated or remyelinated in vitro according to the methods disclosed.

An EP2 agonist which may have an EP3 agonistic effect has an effect of regenerating and / or protecting nerves, and is therefore useful as a therapeutic agent for a disease of the peripheral nervous system, such as a lower or upper motor neuron disease, a nerve root disease, plexopathy, thoracic outlet compression syndrome, peripheral neuropathy, neurofibromatosis and neuromuscular transmission disease. An EP2 agonist which has an EP3 agonistic effect is a safe and effective agent for the regeneration and / or protection of nerves which has little influence on the circulatory system.

The invention belongs to the research and development field of neuro-protective medicament, and discloses a traditional Chinese medicine monomer capable of promoting growth of motoneuron. In the aspect of isolated cell level, the traditional Chinese medicine compound, can obviously promote enation of motoneuron; in the aspect of integral animal level, the compound can obviously promote functional rehabilitation of impaired sciatic nerve and femoral nerve. The invention can be applied to medicinal development for amyotrophic lateral sclerosis and relevant motoneuro symptoms.

A method for forming neuromuscular junctions includes forming functional neuromuscular junctions between motoneurons and muscle cells by co-culturing one or more human motoneurons and one or more human muscle cells in a substantially serum-free medium. A synthetic mammalian neuromuscular junction includes a human motoneuron functionally linked to a human muscle cell in a substantially serum-free medium. An artificial substrate may be used to support the one or more neuromuscular junctions.

The present invention relates to the treatment of motoneuron diseases. More particularly the invention relates to the treatment of amyotrophic lateral sclerosis (ALS). It is found that the intracerebroventricular delivery of low amounts of vascular endothelial growth factor into a preclinical ALS animal model induces a significant motor performance and prolongation of survival time of said animals.

The present invention relates to the treatment of motoneuron diseases. More particularly the invention relates to the treatment of amyotrophic lateral sclerosis (ALS). It is found that the intracerebroventricular delivery of low amounts of vascular endothelial growth factor into a preclinical ALS animal model induces a significant motor performance and prolongation of survival time of said animals.

The present invention relates to rectal administration of phenylbutyrate for treating a motor neuron disease, such as, for example, spinal muscular atrophy or a metabolic disease such as, for example, an urea cycle disorder, related methods and compositions.

The invention discloses a wild-type p53-induced protein phosphatase 1 gene (Wip1) and a purpose of its expressed protein in the treatment of amyotrophic lateral sclerosis. The in-vivo experiment demonstrates that the expression of Wip1 in SOD1G93A ALS mice is significantly decreased and is closely related to the occurrence and development of the disease, overexpression of Wip1 gene can be regulated and controlled in neuronal cells through the gene, and the neuronal survival can be survived by inhibiting a DNA damage response mechanism, which can suggest that high expression of the proto-oncogene Wip1 can treat amyotrophic lateral sclerosis. The present invention also discloses the polymer nanoparticles for treating amyotrophic lateral sclerosis by administering motoneurons that target thebrain and spinal cord of a subject. The Wip1 gene provides a novel technical means for the prevention and treatment of amyotrophic lateral sclerosis.

The present invention relates to culture systems comprising differentiated stem cells, that may be used for identifying agents useful in treating degenerative nervous system disorders and are suitable for high-throughput screening applications. It is based, at least in part, on the discovery that co-cultures of (i) astrocytes expressing a mutated SODI gene and (ii) stem-cell derived motor neurons manifested cell death via a Bax-dependent mechanism, and modeled motor neuron death in amyotrophic lateral sclerosis.

The invention presents a therapeutic agent (and progress suppressant) for amyotrophic lateral sclerosis (ALS) containing HGF and / or HGF gene as active ingredient. HGF has an effect of improving the motor function of ALS and life span through two actions, that is, direct neuronutrient factor activity on motoneurons, and indirect improving action of glutamate cytotoxicity on motoneurons by maintaining the level of glutamate transporter in astrocytes. Hence, HGF and / or HGF gene can be used as an effective therapeutic agent not known in the past.

The present invention relates to a novel compound useful as a TRPV4 antagonist, specifically the compound 1-(((5S,7R)-3-(5-cyclopropylpyrazin-2-yl)-7-hydroxy-2-oxo-1-oxa-3-azaspiro[4.5]decan-7-yl)methyl)-1H-benzo[d]imidazole-6-carbonitrile, pharmaceutically acceptable salts thereof and pharmaceutical compositions containing the compound. The compound of the invention can be useful in the treatmentof a disease state selected from: atherosclerosis, disorders related to vasogenic edema, postsurgical abdominal edema, ocular edema, cerebral edema, local and systemic edema, fluid retention, sepsis,hypertension, inflammation, bone related dysfunctions and congestive heart failure, pulmonary disorders, chronic obstructive pulmonary disorder, ventilator induced lung injury, high altitude inducedpulmonary edema, acute respiratory distress syndrome, acute lung injury, pulmonary fibrosis, sinusitis / rhinitis, asthma, cough; including acute cough, sub-acute cough and chronic cough, pulmonary hypertension, overactive bladder, cystitis, pain, motor neuron disorders, genetic gain of function disorders, cardiovascular disease, renal dysfunction, stroke, glaucoma, retinopathy, endometriosis, pre-term labor, dermatitis, pruritus, pruritus in liver disease, diabetes, metabolic disorder, obesity, migraine, pancreatitis, tumor suppression, immunosuppression, osteoarthritis, crohn's disease, colitis, diarrhea, intestinal irregularity (hyperreactivity / hyporeactivity), fecal incontinence, irritable bowel syndrome (IBS), constipation, intestinal pain and cramping, celiac disease, lactose intolerance, and flatulence.

The present invention provides a C-terminal CDNF fragment sequence or a sequence which has at least 80% homology or sequence identity to said sequence. The C-terminal CDNF fragment protects ER stressed neurons, motoneurons and dopaminergic neurons and the fragment is capable of penetrating neuronal cell membrane as well as the blood-brain-barrier. The present invention further provides said fragment and pharmaceutical compositions comprising said fragment for use in treatments of degenerative diseases and disorders including central nervous system diseases, diabetes and retinal disorders. The present invention is also providing a C-terminal MANF fragment sequence or a sequence which has at least 80% homology or sequence identity to the said sequence and pharmaceutical compositions comprising said MANF fragment for use in the treatment of degenerative diseases and disorders including central nervous system diseases, diabetes and retinal disorders.

The invention disclosed herein describes a novel therapeutic target for motoneuron diseases (altered dynamics of microtubules in neurons); a method for measuring the state of activity of this therapeutic target in subjects with established, incipient, or potential motoneuron disease; the discovery of drug agents that modulate neuronal microtubule dynamics in living subjects with motoneuron diseases; the discovery that administration of such agents, alone or in combinations, can provide marked neuroprotective therapy for living subjects with motoneuron diseases including delay in symptoms and prolongation of survival; and the discovery that monitoring of neuronal microtubule dynamics in subjects with motoneuron diseases, in response to therapeutic interventions, allows diagnostic monitoring for optimization of therapeutic regimen and strategy for individual subjects or for drug trials.

A method includes applying thrombin and salmon fibrinogen to injured motor neurons at a central nervous system injury site, thereby enhancing repair and functional recovery of the injured motor neurons, such as by injecting or spraying thrombin and salmon fibrinogen to form a fibrin clot, or by applying a composition including thrombin and salmon fibrinogen. A method of promoting the functional recovery of a patient who has suffered a central nervous system injury includes this method. A composition including thrombin and salmon fibrinogen is adapted to be applied to injured motor neurons at a central nervous system injury site, thereby enhancing repair and functional recovery of the injured motor neurons.

The invention disclosed herein describes a novel therapeutic target for motoneuron diseases (altered dynamics of microtubules in neurons); methods for measuring the state of activity of this therapeutic target in subjects with established, incipient, or potential motoneuron disease; the discovery of drug agents that modulate neuronal microtubule dynamics in living subjects with motoneuron diseases; the discovery that administration of such agents, alone or in combinations, can improve MT-mediated transport of ''cargo'' molecules along and through axons; the discovery that such modulation of altered microtubule dynamics and improvement in MT-transport of molecules along axons can provide marked neuroprotective therapy for living subjects with motoneuron diseases, including delay in symptoms and prolongation of survival; and the discovery that monitoring of neuronal microtubule dynamics in response to therapeutic interventions in subjects with motoneuron diseases,, allows diagnostic monitoring, to optimize therapeutic regimens and treatment strategies in individual subjects or in drug trials.

The present invention is directed to new compositions uses thereof and related methods for the treatment of a motoneuron disease or disorder. In particular, the invention relates to the new use of IFNγ antagonists or viral vectors, uses, compositions thereof and related methods for the treatment of motoneuron disease or disorder such as ALS.

The present invention relates to a bicistronic expression vector for silencing a gene specifically in astrocytes and neurons, comprising two expression cassettes comprising a first and a second silencer sequence, respectively, wherein the expression of said first silencer sequence within astrocytes is regulated by an astrocyte-specific promoter and the expression of said second silencer sequence within neurons is regulated by a neuron-specific promoter. In a preferred embodiment, said first and second silencer sequences are SOD1 silencer sequences. Pharmaceutical composition comprising said bicistronic vector and the use of the same in the treatment of motoneuron diseases are further described.

The invention provides a method of co-culturing mammalian muscle cells and mammalian motoneurons. The method comprises preparing one or more carriers coated with a covalently bonded monolayer of trimethoxysilylpropyl diethylenetriamine (DETA); suspending isolated fetal mammalian skeletal muscle cells in serum-free medium according to medium composition 1; suspending isolated fetal mammalian spinal motoneurons in serum-free medium according to medium composition 1; plating the suspended muscle cells onto the one or more carriers at a predetermined density and allowing the muscle cells to attach; plating the suspended motoneurons at a predetermined density onto the one or more carriers and allowing the motoneurons to attach; covering the one or more carriers with a mixture of medium composition 1 and medium composition 2; and incubating the carriers covered in the media mixture.

The invention disclosed herein describes a novel therapeutic target for motoneuron diseases (altered dynamics of microtubules in neurons); methods for measuring the state of activity of this therapeutic target in subjects with established, incipient, or potential motoneuron disease; the discovery of drug agents that modulate neuronal microtubule dynamics in living subjects with motoneuron diseases; the discovery that administration of such agents, alone or in combinations, can improve MT-mediated transport of “synaptic vesicle cargo” molecules along and through axons; the discovery that such modulation of altered microtubule dynamics and improvement in MT-transport of molecules along axons can provide marked neuroprotective therapy for living subjects with motoneuron diseases, including delay in symptoms and prolongation of survival; and the discovery that monitoring of neuronal microtubule dynamics in response to therapeutic interventions in subjects with motoneuron diseases, allows diagnostic monitoring, to optimize therapeutic regimens and treatment strategies in individual subjects or in drug trials. The monitoring involves measuring isotope enrichment in secreted synaptic vesicle cargo molecules.