45 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 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.

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.

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.

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 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 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.