Abstract: Carbamathione agent protects brain tissue exposed to a cerebral ischemia/reperfusion injury, and minimizes the size of infarcts that develop as a result of the injury.

Abstract: Carbamathione agent protects brain tissue exposed to a cerebral ischemia/reperfusion injury, and minimizes the size of infarcts that develop as a result of the injury.

Abstract: Granulocyte colony-stimulating factor (G-CSF; a stem cell enhancer and facilitator), DETC-MeSO (a glutamate receptor partial antagonist and anti-excitotoxicity agent), and sulindac (a potent anti-oxidant and anti-inflammatory agent) each can protect brain tissue exposed to a cerebral ischemia/reperfusion injury, and minimize the size of infarcts that develop as a result of the injury. When administered in combination, these agents are effective at protecting brain tissue and minimizing the size of an infarct resulting from the injury at much lower concentrations compared to using a single agent.

Abstract: Gene therapy using expression vectors containing a granulocyte colony-stimulating factor (GCSF) gene are able to protect cells in a cell-based as well as animal-based models for ischemic stroke

Abstract: Granulocyte colony-stimulating factor (G-CSF; a stem cell enhancer and facilitator), DETC-MeSO (a glutamate receptor partial antagonist and anti-excitotoxicity agent), and sulindac (a potent anti-oxidant and anti-inflammatory agent) each can protect brain tissue exposed to a cerebral ischemia/reperfusion injury, and minimize the size of infarcts that develop as a result of the injury. When administered in combination, these agents are effective at protecting brain tissue and minimizing the size of an infarct resulting from the injury at much lower concentrations compared to using a single agent.

Abstract: Granulocyte colony-stimulating factor (G-CSF; a stem cell enhancer and facilitator), DETC-MeSO (a glutamate receptor partial antagonist and anti-excitotoxicity agent), and sulindac (a potent anti-oxidant and anti-inflammatory agent) each can protect brain tissue exposed to a cerebral ischemia/reperfusion injury, and minimize the size of infarcts that develop as a result of the injury. When administered in combination, these agents are effective at protecting brain tissue and minimizing the size of an infarct resulting from the injury at much lower concentrations compared to using a single agent.

Abstract: Granulocyte colony-stimulating factor (G-CSF; a stem cell enhancer and facilitator), DETC-MeSO (a glutamate receptor partial antagonist and anti-excitotoxicity agent), and sulindac (a potent anti-oxidant and anti-inflammatory agent) each can protect brain tissue exposed to a cerebral ischemia/reperfusion injury, and minimize the size of infarcts that develop as a result of the injury. When administered in combination, these agents are effective at protecting brain tissue and minimizing the size of an infarct resulting from the injury at much lower concentrations compared to using a single agent.

Abstract: Granulocyte colony-stimulating factor (G-CSF; a stem cell enhancer and facilitator), DETC-MeSO (a glutamate receptor partial antagonist and anti-excitotoxicity agent), and sulindac (a potent anti-oxidant and anti-inflammatory agent) each can protect brain tissue exposed to a cerebral ischemia/reperfusion injury, and minimize the size of infarcts that develop as a result of the injury. When administered in combination, these agents are effective at protecting brain tissue and minimizing the size of an infarct resulting from the injury at much lower concentrations compared to using a single agent.

Abstract: Granulocyte colony-stimulating factor (G-CSF; a stem cell enhancer and facilitator), DETC-MeSO (a glutamate receptor partial antagonist and anti-excitotoxicity agent), and sulindac (a potent anti-oxidant and anti-inflammatory agent) each can protect brain tissue exposed to a cerebral ischemia/reperfusion injury, and minimize the size of infarcts that develop as a result of the injury. When administered in combination, these agents are effective at protecting brain tissue and minimizing the size of an infarct resulting from the injury at much lower concentrations compared to using a single agent.

Abstract: Granulocyte colony-stimulating factor (G-CSF; a stem cell enhancer and facilitator), DETC-MeSO (a glutamate receptor partial antagonist and anti-excitotoxicity agent), and sulindac (a potent anti-oxidant and anti-inflammatory agent) each can protect brain tissue exposed to a cerebral ischemia/reperfusion injury, and minimize the size of infarcts that develop as a result of the injury. When administered in combination, these agents are effective at protecting brain tissue and minimizing the size of an infarct resulting from the injury at much lower concentrations compared to using a single agent.

Abstract: Granulocyte colony-stimulating factor (G-CSF; a stem cell enhancer and facilitator), DETC-MeSO (a glutamate receptor partial antagonist and anti-excitotoxicity agent), and sulindac (a potent anti-oxidant and anti-inflammatory agent) each can protect brain tissue exposed to a cerebral ischemia/reperfusion injury, and minimize the size of infarcts that develop as a result of the injury. When administered in combination, these agents are effective at protecting brain tissue and minimizing the size of an infarct resulting from the injury at much lower concentrations compared to using a single agent.

Abstract: The invention relates to the discovery that in an animal model of Parkinson's disease (PD), administration of granulocyte colony-stimulating factor (G-CSF) to rodents having 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced PD restored the function of dopamine neurons. In these animals, G-CSF treatment increased the number of dopamine neurons in the substantia nigra (SN), G-CSF treatment partially restored the nigrostriatal pathway, and G-CSF restored the function of dopamine to the level before MPTP treatment. The invention also relates to the discovery that treatment of a human patient with corticobasilar ganglionic degeneration, a rare progressive neurological disorder characterized by Parkinsonism and coritcal dysfunction, with G-CSF resulted in a significant improvement in the patient's Unified Parkinson's Disease Rating Scale evaluations as well as measures of activity of daily living.

Abstract: The invention relates to the discovery that in an animal model of Parkinson's disease (PD), administration of granulocyte colony-stimulating factor (G-CSF) to rodents having 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced PD restored the function of dopamine neurons. In these animals, G-CSF treatment increased the number of dopamine neurons in the substantia nigra (SN), G-CSF treatment partially restored the nigrostriatal pathway, and G-CSF restored the function of dopamine to the level before MPTP treatment. The invention also relates to the discovery that treatment of a human patient with corticobasilar ganglionic degeneration, a rare progressive neurological disorder characterized by Parkinsonism and coritcal dysfunction, with G-CSF resulted in a significant improvement in the patient's Unified Parkinson's Disease Rating Scale evaluations as well as measures of activity of daily living.

Abstract: Disclosed are novel compounds and novel pharmaceutical compositions for use in medical therapy, as well as intermediates and processes for preparing such compounds. Therapeutic methods for preventing or treating glutamate-related disorders in a mammal and methods to inhibit or prevent glutamate binding in mammalian tissue are also disclosed.

Abstract: Disclosed are novel compounds and novel pharmaceutical compositions for use in medical therapy, as well as intermediates and processes for preparing such compounds. Therapeutic methods for preventing or treating glutamate-related disorders in a mammal and methods to inhibit or prevent glutamate binding in mammalian tissue are also disclosed.

Abstract: Disclosed are novel compounds and novel pharmaceutical compositions for use in medical therapy, as well as intermediates and processes for preparing such compounds. Therapeutic methods for preventing or treating glutamate-related disorders in a mammal and methods to inhibit or prevent glutamate binding in mammalian tissue are also disclosed.

Abstract: A method of using a compound of formula (I) wherein R.sup.1, R.sup.2, R.sup.3, X and n have any of the meanings defined in the specification, to antagonize glutamate binding, or to treat glutamate-related disorders is provided. Novel compounds, intermediates and pharmaceutical compositions are also provided.