Abstract: The invention relates to a method of reducing neuronal injury or apoptosis including administering to a patient in need thereof an effective amount of a p38 mitogen-activated protein kinase (MAPK) inhibitor. Methods of treating an HIV-mediated dementia, glaucoma, or other neurodegenerative disorders are also disclosed.

Abstract: A method for identifying agents useful for protection of a human neuron from injury. The method includes the steps of providing a cell which has NMDA receptor; selecting a agent potentially useful for oxidation of the NMDA receptor; treating the cell with the agent; and determining whether the NMDA receptor is oxidized by the agent.

Abstract: The present invention provides novel aminoadamantane derivatives, methods of making the derivatives, compositions including the novel aminoadamantane derivatives, and methods for the treatment and prevention of neurological diseases using the derivatives and compositions.

Abstract: The invention features methods of treating cytotoxic damage in a subject comprising administering to the subject a substance which is a complement inhibitor, free radical scavenger, or both, to thereby treat cytotoxic damage. The methods of the invention can be used to treat cytotoxic damage associated with a non-thrombotic or thrombotic condition. Methods of treating thrombotic conditions such as stroke and/or ischemia in a subject, comprise administering a thrombolytic agent and a substance which is a complement inhibitor, free radical scavenger or both.

Abstract: Elevated glutamate levels are associated with glaucoma, and damage to retinal ganglion cells can be controlled by administering to the patient a compound capable of reducing glutamate induced excitotoxicity in a concentration effective to cause reduction of such excitotoxicity.

Abstract: The present invention provides novel aminoadamantane derivatives, methods of making the derivatives, compositions including the novel aminoadamantane derivatives, and methods for the treatment and prevention of neurological diseases using the derivatives and compositions.

Abstract: Compounds that inhibit caspase activity, particularly those that bind a caspase substrate and protect it, are combined with a vector such as liposomes or an antennapeida peptide to treat glaucoma.

Abstract: The present invention provides a method of differentiating progenitor cells to produce a population containing protected neuronal cells. A method of the invention includes the steps of contacting the progenitor cells with a differentiating agent; and introducing into the progenitor cells a nucleic acid molecule encoding a MEF2 polypeptide or an active fragment thereof, thereby differentiating the progenitor cells to produce a population containing protected neuronal cells. In one embodiment, the MEF2 polypeptide is human MEF2C or an active fragment thereof.

Abstract: Disclosed is a method for decreasing NMDA receptor-mediated neuronal damage in a mammal by administering to the mammal a nitroso-compound that generates nitric-oxide or related redox species, in a concentration effective to effect neuroprotection. Also disclosed is a method for decreasing NMDA receptor-mediated neuronal damage in a mammal by administering to the mammal a nitroso-compound that generates nitric oxide (or a related redox species such as NO.sup.- or NO.sup.+ equivalent), or a physiologically concentration effective to cause such neuroprotection.

Abstract: Elevated glutamate levels are associated with glaucoma, and damage to retinal ganglion cells can be controlled by administering to the patient a compound capable of reducing glutamate induced excitotoxicity in a concentration effective to cause reduction of such excitotoxicity.

Abstract: Disclosed is a method and patch for decreasing NMDA receptor-mediated neuronal damage in a mammal by administering to the mammal a nitroso-compound that generates nitric-oxide or related redox species, in a concentration effective to effect neuroprotection. Also disclosed is a method for decreasing NMDA receptor-mediated neuronal damage in a mammal by administering to the mammal a nitroso-compound that generates nitric oxide (or a related redox species such as NO.sup.- or NO.sup.+ equivalent), or a physiologically concentration effective to cause such neuroprotection.

Abstract: Disclosed is a method for decreasing NMDA receptor-mediated neuronal damage in a mammal by administering to the mammal a nitroso-compound that generates nitric-oxide or related redox species, in a concentration effective to effect neuroprotection. Also disclosed is a method for decreasing NMDA receptor-mediated neuronal damage in a mammal by administering to the mammal a nitroso-compound that generates nitric oxide (or a related redox species such as NO.sup.- or NO.sup.+ equivalent), or a physiologically concentration effective to cause such neuroprotection.

Abstract: Disclosed is a method for reducing non-ischemic NMDA receptor-mediated neuronal damage in a mammal by administering to the mammal a compound of the formula shown in FIG. 1 (or a physiologically-acceptable salt thereof), wherein R.sub.1 includes an amino group, R.sub.2 -R.sub.17 are independently H or a short chain aliphatic group comprising 1-5 carbons, and R.sub.4 and R.sub.10 also may (independently) be a halogen or an acyl group. Also disclosed is a screen for antagonists of NMDA receptor mediated neurotoxicity which have an enhanced prospect for being clinically tolerated and selective against such neurotoxicity.

Abstract: Damage to CNS neurons of a human patient infected with a human immunodeficiency virus is reduced by administering an antagonist of the NMDA receptor complex.

Abstract: Disclosed is a method for decreasing NMDA receptor-mediated neuronal damage in a mammal by administering to the mammal a nitroso-compound that generates nitric-oxide or related redox species, in a concentration effective to effect neuroprotection. Also disclosed is a method for decreasing NMDA receptor-mediated neuronal damage in a mammal by administering to the mammal a nitroso-compound that generates nitric oxide (or a related redox species such as NO.sup.31 or NO.sup.+ equivalent), or a physiologically concentration effective to cause such neuroprotection.

Abstract: Disclosed is a method for reducing non-ischemic NMDA receptor-mediated neuronal damage in a mammal by administering to the mammal a compound of the formula shown in FIG. 1 (or a physiologically-acceptable salt thereof), wherein R.sub.1 includes an amino group, R.sub.2 -R.sub.17 are independently H or a short chain aliphatic group comprising 1-5 carbons, and R.sub.4 and R.sub.10 also may (independently) be a halogen or an acyl group. Also disclosed is a screen for antagonists of NMDA receptor mediated neurotoxicity which have an enhanced prospect for being clinically tolerated and selective against such neurotoxicity.

Abstract: Disclosed is a method for reducing NMDA receptor-mediated neuronal damage in a mammal by administering to the mammal a nitric-oxide generating compound, or a physiologically acceptable salt thereof, in a concentration effective to cause such reduction. Also disclosed is a method for reducing NMDA receptor-mediated neuronal damage in a mammal by administering to the mammal nitroprusside, nitroglycerin, or a derivative of one of those compounds, in a concentration effective to cause such reduction.

Abstract: A method of reducing death of CNS neurons in a human patient infected with a human immunodeficiency virus, involving administering to the patient a compound capable of reducing the gp120-responsive rise in free Ca.sup.++ ion concentration in the CNS neurons of the patient, in a concentration effective to cause such reduction.

Abstract: A method of measuring the beta-hydroxybutyrate concentration of a urine sample including, in one step, the oxidation of beta-hydroxybutyrate to acetone and acetoacetate and the removal of pre-existing acetone/acetoacetate.