62 results about "Glutamate receptor" patented technology

A peptide containing 24 amino acid residues that binds to anti-neuronal-glutamate-receptor autoantibodies associated with Rasmussen's encephalitis and that blocks activation of the GluR3 subunit is described. Methods of making the peptide and treating Rasmussen's encephalitis are also disclosed. Autoantibodies to other glutamate receptor subunits are associated with paraneoplastic neurodegenerative disease, amyotrophic lateral sclerosis, and neurodegenerative disease of unknown diagnosis. Methods of screening patients and of monitoring patients being treated for these disorders and syndromes are further described.

The present invention relates to biologically active peptides derived from the neurite outgrowth-promoting domain of luminin-1, i.e. the γ1-chain of laminin-1. These peptides include the decapeptide RDIAEIIKDI (SEQ ID NO: 1) and the truncated peptides derived therefrom comprising the biologically active domain thereof, the tripeptide KDI. The invention is directed to the biologically active tripeptide motifKDI, and to its use in promoting regeneration of neuronal or non-neuronal tissues and, in specific, to its use in the treatment of spinal cord injuries.

This invention discloses that a combination of two drugs, from two different and previously unrelated categories, provides effective and long-lasting relief from neuropathic pain. Both drugs can be taken orally, in a convenient, painless, non-invasive manner that does not require injections. One drug in this combination is an alpha2 adrenergic agonist, exemplified by clonidine. The other drug in the pain-relieving combination has a tri-cyclo-alkyl-amine (TCAA) structure. At least some TCAA drugs have antagonist (receptor-blocking) activity at two entirely different classes of neuronal receptors: the muscarinic subclass of acetylcholine (ACh) receptors, and the NMDA subclass of glutamate receptors. Such drugs include ethopropazine, normally used as an anti-cholinergic drug, and desipramine, normally used as an anti-depressant. Tests by the Applicants have shown that at least some TCAA drugs can relieve neuropathic pain to a limited extent, but at the doses required to relieve pain, they cause adverse side effects, and any pain relief is relatively brief and short-lived. However, when a TCAA drug such as ethopropazine is administered together with an alpha2 adrenergic agonist such as clonidine, these drugs mutually potentiate one another's neuropathic pain-relieving action, and provide potent and sustained neuropathic pain relief, even when each agent is administered at a low dosage that is below its threshold for causing adverse side effects. Accordingly, this drug combination can provide safe and effective relief of neuropathic pain and possibly other types of chronic and / or intractable pain, at dosages which are so low that they do not pose serious risks of adverse side effects.

The present invention relates to a method for diagnosing neuroendocrine cancers via detecting the presence of N-methyl D-asparate-associated (NMDA) glutamate receptors type 1 and / or type 2. Methods for preventing and treating neuroendocrine cancers are also disclosed.

There is provided a biosensor capable of increasing a detecting sensitivity of a target substance of glutamate, by using a nano wire having excellent electrical characteristics and by immobilizing a receptor of glutamate to be detected on a substrate which is disposed between a nano wire and another nano wire and a method for manufacturing the same. The biosensor for detecting glutamate according to the present invention can be manufactured with an arrangement in which the nano wire is selectively arranged on a solid substrate in a matrix. Since this biosensor can prevent the degradation of the nano wire in the electrical characteristic, it can sensitively detect glutamate even through a small amount thereof is contained in a food so that it can be effectively used in detecting the food additive existing in the processed foodstuffs.

The present invention provides a synthetic regulator of glutamate receptor function, which regulator is a light-sensitive (photoreactive) regulator. The present invention further provides a light-regulated glutamate receptor that includes a subject synthetic regulator non-covalently associated with the glutamate receptor. Also provided are cells and membranes comprising a subject light-regulated glutamate receptor. The present invention further provides methods of modulating glutamate receptor function, involving use of light. The present invention further provides methods of identifying agents that modulate glutamate receptor function.

The present invention relates to methods of therapy for substance addiction comprising the administration to a subject in need thereof a combination of: (i) a mu-opioid receptor antagonist; (ii) a calcium channel blocker which is long-acting or in sustained-release form or which is nimodipine in rapid release form; and (iii) an NMDA glutamate receptor modulator; as well as combinations, kits and composition useful therefor.

Prolonged administration of subanesthetic dosages of ketamine, which suppresses activity at NMDA receptors, can provide a damaged central nervous system with an opportunity to use its innate healing processes to “reset” NMDA receptors which were pushed into an unwanted hyper-sensitized state by unusually high activity. However, such treatments can cause permanent brain damage, if the ketamine dosage is too heavy or prolonged. Certain types of “safener” drugs have previously been identified, which can block or at least reduce those unwanted side effects. It is disclosed that if two classes of safener drugs are combined, which will simultaneously suppress activity at both (i) muscarinic acetylcholine receptors, and (ii) the kainate and AMPA classes of glutamate receptors, those safener drug combinations can provide exceptionally potent and reliable safening activity, which can enable the safe use of potent NMDA antagonist drugs for a number of highly beneficial purposes.

The invention provides a method for screening a nucleic acid suppression molecule for effectively suppressing the expression of a brain eIF6 gene from in-vitro cultured cells on the basis of the effect of eIF6 on negative regulation of memory and enhancement on glutamate receptor expression, the nucleic acid inhibition molecule screened by the method, and an application of the nucleic acid inhibition molecule in preventing and / or treating exercise-induced fatigue and / or forgetfulness and related diseases.

This invention relates to novel aryl ureido benzoic acid derivatives useful as selective and non-competitive antagonists of the ionotropic GluR5 receptor. Due to their biological activity, the aryl ureido derivatives of the invention are considered useful for treating diseases that are responsive to modulation of an aspartate or a glutamate receptor. Moreover the invention provides chemical compounds for use according to the invention, as well as pharmaceutical compositions comprising the chemical compounds, and methods of treating diseases or disorders or conditions responsive to modulation of an aspartate or a glutamate receptor.

The present invention relates to a method of treatment of Parkinson's disease, and to the use of antisense oligonucleotides or triplex oligonucleotides introduced into targeted brain structures to decrease the function of brain circuits known to be overactive in the Parkinsonian brain. Antisense or triplex oligonucleotides are targeted to the internal globus pallidus and / or substantia nigra pars reticulata (SNr) where the expression of glutamic acid decarboxylase (GAD67, GAD65, or a combination of the two isoforms) is downregulated. The present invention also relates to a method of treatment of Parkinson's disease where antisense or triplex oligonucleotides are targeted to the internal globus pallidus and / or substantia nigra pars reticulata for the downregulation of glutamate receptors. The present invention further relates to a method of treatment of Parkinson's disease where antisense or triplex oligonucleotides are targeted to the thalamic motor nuclei for the downregulation of GABA receptors.

The present invention relates to a method for diagnosing neuroendocrine cancers via detecting the presence of N-methyl D-asparate-associated (NMDA) glutamate receptors type 1 and / or type 2. Methods for preventing and treating neuroendocrine cancers are also disclosed.

The invention provides a method of screening patients to identify those patients more likely to exhibit an increased risk of treatment-emergent suicidal ideation comprising: (a) obtaining a sample of genetic material from the patients, and (b) assaying the sample for the presence of a genotype in the patients which is associated with an increased risk of treatment-emergent suicidal ideation, wherein the genotype is characterized by a polymorphism in a gene selected from the group consisting of glutamine receptor, ionotropic, kainate 2 (GRIK2); glutamate receptor ionotropic AMPA 3 (GRIA3); and combinations thereof.

The present invention relates to novel nucleic acid ligands or aptamers that demonstrate potent and selective inhibition of the open-channel conformation of the α-amino-3-hydroxy-5-methyl-4-isoxazole propionate (AMPA) subtype of ionotropic glutamate receptors.

The inventive subject matter relates to a glutamate receptor, DNA which encodes the receptor, a transformed cell expressing the receptor, a method for producing the receptor, a method for identifying an agonist, antagonist, or allosteric modulator for glutamic acid, a method for identifying an agonist for glutamic acid, an antibody to the receptor, and processes for making glutamate receptor modulators and pharmaceutical compositions comprising said modulator.

Fertilized egg isolate, methods for preparing the fertilized egg isolate and uses thereof for treating mental health disorders and disease or conditions mediated by or associated with one or more glutamate receptors or by the neurokinin 2 (NK2) receptor.

The present invention relates to a method for diagnosing neuroendocrine cancers via detecting the presence of N-methyl D-asparate-associated (NMDA) glutamate receptors type 1 and / or type 2. Methods for preventing and treating neuroendocrine cancers are also disclosed.