85 results about "Excitotoxicity" patented technology

A method of inhibiting the binding between N-methyl-D-aspartate receptors and neuronal proteins in a neuron is disclosed. The method comprises administering to the neuron an effective inhibiting amount of a peptide replacement agent for the NMDA receptor or neuronal protein interaction domain that effect said inhibition of the NMDA receptor—neuronal protein interaction. The method is of value in reducing the damaging effect of injury to mammalian cells. Postsynaptic density-95 protein (PSD-95) couples neuronal N-methyl-D-aspartate receptors (NMDARs) to pathways mediating excitotoxicity, ischemic and traumatic brain damage. This coupling was disrupted by transducing neurons with peptides that bind to modular domains on either side of the PSD-95/NMDAR interaction complex. This treatment attenuated downstream NMDAR signaling without blocking NMDAR activity, protected cultured cortical neurons from excitotoxic insults, dramatically reduced cerebral infarction volume in rats subjected to transient focal cerebral ischemia, and traumatic brain injury (TBI) in rats.

This invention describes the administration of multiple therapeutic agents with insulin in conjunction with bexarotene, ketamine, monoclonal antibodies Etanercept, IGF-1, and acetylcholine esterase inhibitors physostigmine, for treatment of Alzheimer's disease and other neurodegenerative diseases. Insulin, improves memory; also augments and amplifies the effects of the adjuvant therapeutic agents (paracrine and intracrine effects) and consequently reduces the β amyloid, its soluble precursors, prevents damage to the neuronal skeletal network (taupathy), and blocks glutamate excitotoxicity, reduces brain inflammation, prevents apoptosis, and increases the acetylcholine levels in the neurons and synapses; by using a combination of insulin, bexarotene, ketamine, Etanercept, IGF-1, and physostigmine therapeutic agents. The results are achieved by using the specially designed Iontophoresis incorporated olfactory mucosal delivery (ORE) catheter device located at the olfactory nerves, sphenoid sinus, and adjacent structures described here, to transport the large molecules of therapeutic agents to treat AD delivered to the CNS bypassing BBB from ORE.

The invention relates to methods for the prevention and/or treatment of tinnitus induced by cochlear excitotoxicity. In these methods, a pharmaceutical composition comprising an NMDA receptor antagonist is administered to an individual in need of such treatment by appropriate devices and/or formulations for local administration to the inner ear. The tinnitus to be prevented and/or treated may be provoked by acoustic trauma, presbycusis, ischemia, anoxia, sudden deafness, or other cochlear excitotoxic-inducing occurrence.

The present invention relates to novel compounds that are A_2A adenosine receptor antagonists, and to their use in treating mammals for various disease states, such as obesity, CNS disorders, including the “movement disorders” (Parkinson's disease, Huntington's Chorea, and catelepsy), and cerebral ischemia, excitotoxicity, cognitive and physiological disorders, depression, ADHD, and drug addiction (alcohol, amphetamine, cannabinoids, cocaine, nicotine, and opioids) and to their use in the enhancement of immune response. The invention also relates to methods for the preparation of such compounds, and to pharmaceutical compositions containing them.

The present invention relates to compositions and methods for the treatment of neurological disorders related to glutamate excitotoxicity and Amyloid β toxicity. More specifically, the present invention relates to novel combinatorial therapies of Multiple Sclerosis, Alzheimer's disease, Alzheimer's disease related disorders, Amyotrophic Lateral Sclerosis, Parkinson's disease, Huntington's disease, neuropathic pain, alcoholic neuropathy, alcoholism or alcohol withdrawal, or spinal cord injury.

The present invention relates to combinations and methods for the treatment of neurological disorders related to glutamate excitotoxicity and Amyloid β toxicity. More specifically, the present invention relates to novel combinatorial therapies of Multiple Sclerosis, Alzheimer's disease, Alzheimer's disease related disorder, Amyotrophic Lateral Sclerosis, Parkinson's disease, Huntington's disease, neuropathic pain, alcoholic neuropathy, alcoholism or alcohol withdrawal, or spinal cord injury, based on Baclofen and Acamprosate combination.

The present invention relates to an excitotoxicity related injury treatment peptide, and provides a peptide containing an amino acid sequence YEKLLDTEI (SEQ ID NO:1) or a functional variant thereof, wherein the peptide is an active peptide for treating central nervous system injury. The invention further provides a chimeric peptide containing the active peptide and an internalized peptide. The present invention further provides a pharmaceutical composition containing the active peptide or the chimeric peptide, and medical applications of the active peptide or the chimeric peptide.

A method of inhibiting excitotoxicity by indirectly activating α4β2 nicotinic acetylcholine receptors (nAChRs) which indirectly activate synaptic AMPA and NMDA receptors is disclosed. Inhibitors of α7 nACHRs, such as macrocyclic diterpenoids, more specifically cembranoids or methyllycaconitine (MLA), indirectly activate α4β2 nAChRs and can be used to treat neurodegenerative diseases, including, but not limited to, Alzheimer's Disease, Parkinson Disease, AIDS related dementia and the delayed effects of stroke. They can also be used to treat diseases associated with neuronal impairment, including, but not limited to glaucoma caused by optical nerve damage, delayed effects of epilepsy; and multiple sclerosis.

The c-Jun NH₂-terminal kinase (JNK) group of MAP kinases are activated by exposure of cells to environmental stress. The role of JNK in the brain was examined by targeted disruption of the gene that encodes the neuronal isoform JNK3. It was found that JNK3 is required for the normal response to seizure activity. Methods of screening for molecules and compounds that decrease JNK3 expression or activity are described. Such molecules or compounds are useful for treating disorders involving excitotoxicity such as seizure disorders, Alzheimer's disease, Huntington disease, Parkinson's disease, and ischaemia.

Deep Brain Stimulation (DBS) is taking off and will be part of the main treatment for brain diseases such as movement disorders, epilepsy, psychiatric diseases and many others. There is a need for more sophisticated devices that can do more in one penetration, not just stimulate. Once there is a probe in the brain, it is used for multiple passive measurements, without harming the brain further. It provides better understanding the brain and real time closed loop improved treatment. An apparatus and method are disclosed, which allow simultaneous monitoring of multiple parameters inside the human brain, such as: pH, temperature, pressure, seizure activity (EEG), degree of metabolism, oxygen tension in the brain, degree of excitotoxicity and others. The ability to measure those parameters during treatment and stimulation procedures makes the difference between success and failure of the patient.

The invention is suitable for the technical field of traditional Chinese medicines, provides application of free sulfur in preparing drug treatment and rehabilitation medicaments and also provides a drug treatment and rehabilitation Chinese herbal composition of which crude drugs include a sulfur element and at least one Chinese herbal component, wherein the weight percentage of the sulfur element to the Chinese herbal component is (0.1-99):(99-0.1); the sulfur element is the free sulfur, sublimed sulfur, precipitated sulfur, sulphion or a sulfocompound. The free sulfur is applied to the preparation of the drug treatment and rehabilitation medicaments, can block the euphoria brought by drugs and can bring a long-efficient and secondary taking prevention effect. A Chinese herbal preparation prepared from the Chinese herbal composition provided by the invention has favorable curative effect for opioid drugs, excitotoxicity drugs and various controlled substances and has stronger inhibitory action for heroin dependent patients longing for the drugs, a certain inhibitory action in the euphoria generated by opioid substances, better curative effect for protracted withdrawal syndrome and action in promoting the restoring of physiological functions of organisms.

The N-alkylglycine trimeres (I), where R1, R2 and R3, independent of one another, are chosen from amongst cyclopropyl, sec-butyl, 2-metoxyethyl, 3-methylbutyl, cyclohexyl, 2-(N-pyrrolidinyl)ethyl, 2-(methylcarbonylamine)ethyl, 3-(2-oxo-N-pyrrolidinyl)propyl, 2-(2-pyridyl)ethyl, phenylethyl, 1-(2-tetrahydrofuryl)methyl, 2-(N-imidazolyl) ethyl, 2-(4-metoxyphenyl) ethyl, 2-(3,4-dimetoxyphenyl) ethyl, 2-(2,4-dichlorophenyl) ethtyl, 2-[2-(N-methyl) pyrrolidinyl] ethyl, 2-(4-aminosulfonylphenyl) ethyl, 2-(morpholine) ethyl, 3-(N,N-diethylamine) propyl, 3,3-diphenylpropyl, 3-(N,N-dimethylamine) propyl, and 2-(N,N-diethylamine) ethyl, their stereoisomeric forms and their mixtures, which are capable of blocking L-glutamate receptors and are useful for treating disorders mediated by said receptors.

The present invention relates to novel compounds that are A_2A adenosine receptor antagonists, and to their use in treating mammals for various disease states, such as CNS disorders, including the “movement disorders” (Parkinson's disease, Huntington's Chorea, and catalepsy), and cerebral ischemia, excitotoxicity, cognitive and physiological disorders, depression, ADHD, hepatic fibrosis, cirrhosis of the liver, and drug addiction (alcohol, amphetamine, cannabinoids, cocaine, nicotine, and opioids) and to their use in the enhancement of immune response. The invention also relates to methods for the preparation of such compounds, and to pharmaceutical compositions containing them.

A process, method, and devices thereof for the rapid destruction of cancer tumor(s) which are made up of thousands to millions of living malignant cancer cells. Such an approach seeks to kill said tumor(s) by causing apoptosis or excitotoxicity and/or osmotic-shock within a human or animal for medical treatment.

The invention relates to a nano-drug for preventing or treating cerebral ischemia-reperfusion injury as well as a preparation method and application of the nano-drug. Cerebral ischemia is a cerebrovascular disease which has the greatest threat to human beings, and oxidative injury, inflammatory response and subsequent excitotoxic cell death can be caused by reperfusion as soon as possible. According to the nano-drug, dopamine is oxidized under an alkaline condition to form dopamine quinone, the dopamine quinone is further oxidized to form polydopamine nanoparticles with supramolecular structures, the formed particles are smooth and round in surface, good in sphericity degree and uniform in particle size distribution, a good dispersion state is kept in a solution, and through in-vitro and in-vivo experiments, the polydopamine nanoparticles prove the biological safety. Application of the polydopamine nanoparticles to a cerebral ischemia model shows that the polydopamine nanoparticles canrelieve cerebral ischemia-reperfusion injury, inhibit inflammatory reaction, inhibit activation of an NF-kappa B signal channel and inhibit excessive activation of microglial cells, and have the potential of inhibiting cerebral inflammatory reaction and relieving cerebral ischemia-reperfusion injury.

The present invention relates to compositions and methods for the treatment of neurological disorders related to glutamate excitotoxicity and Amyloid beta toxicity. More specifically, the present invention relates to novel combinatorial therapies of Multiple Sclerosis, Alzheimer's disease, Alzheimer's disease related disorders, Amyotrophic Lateral Sclerosis, Parkinson's disease, Huntington's disease, neuropathic pain, alcoholic neuropathy, alcoholism or alcohol withdrawal, or spinal cord injury.

The present invention discloses the combined treatment of memantine (N-methyl-D-aspartate receptor antagonist) and tea polyphenol (an antioxidant and anti-inflammatory agent) is more effective (synergistic) in neuroprotection than either memantine or tea polyphenol alone in mouse excitotoxic injury. These findings provide useful information about the potential application of memantine and tea polyphenols in preventing or treating clinical excitotoxic injury such as brain trauma, brain ischemia, epilepsy, and Alzheimer's disease.