Abstract: The present invention relates to the development of a pharmacological non-human animal model that associates memory loss to histopathological features found in the brain of a subject having Alzheimer's Disease. In one embodiment, a four-week continuous infusion of a Fe2+, A?42 and buthionine sulfoximine (FAB) solution in the left ventricle of young adult Long-Evans rats induced memory impairment accompanied by increased hyperphosphorylated Tau protein levels in cerebrospinal fluid. Brains from treated animals displayed neuritic plaques, tangles, neuronal loss, astrogliosis and microgliosis in hippocampus and cortex. The present invention may be utilized in evaluating preventive, therapeutic and diagnostic means for neurologic diseases.

Abstract: The invention provides a therapeutic method for treating at least one symptom of a neurological disorder or disease such as Alzheimer's disease in a mammal, such as a human, wherein the toxicity of a pathogen of ? amyloid peptide and/or glutamate in mammalian cells is implicated and inhibition of the subsequently-induced pathological pathways is desired comprising administering to a mammal in need of such therapy, an effective amount of an N-arylamide or an (N-aminoalkyl)benzamide, including pharmaceutically acceptable salts thereof.

Abstract: The invention provides a therapeutic method for treating at least one symptom of Alzheimer's disease in a mammal, such as a human, wherein the toxicity of a pathogen of ? amyloid peptide mammalian cells is implicated and inhibition of the subsequently-induced pathological pathways is desired comprising administering to a mammal in need of such therapy, an effective amount of a benzoylpiperazine derivative, including pharmaceutically acceptable salts thereof.

Abstract: A novel method for treating a mammal exposed to an exogenous neurotoxic agent is disclosed.

Abstract: The invention provides a therapeutic method for preventing or treating a pathological condition or symptom in a mammal, such as a human, wherein the infectivity of a pathogen such as a retrovirus toward mammalian cells is implicated and inhibition of its infectivity is desired comprising administering to a mammal in need of such therapy, an effective amount of a benzoylquinuclidine derivative that inhibits pathogenic infectivity, including pharmaceutically acceptable salts

Abstract: The invention provides a therapeutic method for preventing or treating a pathological condition or symptom in a mammal, such as a human, wherein the infectivity of a pathogen such as a retrovirus toward mammalian cells is implicated and inhibition of its infectivity is desired comprising administering to a mammal in need of such therapy, an effective amount of procaine, procainamide or an analog thereof that inhibits pathogenic infectivity, including pharmaceutically acceptable salts thereof.

Abstract: A novel compound and method for preventing or treating neurodegenerative diseases by inhibiting acetylcholinesterase and binding the sigma-1 receptor are disclosed. Dimethylcarbamic acid 2,3-bis-dimethylcarbamoyloxy-6-[4-(4-ethyl-piperazin-yl)-butyryl]-phenyl ester and its derivatives represent a novel therapeutic strategy against ?-amyloid peptide induced neurotoxicity, in inhibiting acetylcholinesterase, in improving cholinergic transmission, in binding the sigma-1 receptor, and in releasing a metabolite that is active both as a sigma-1 receptor ligand and an antioxidant.

Abstract: The present invention relates to cortisol-modulating compounds, including but not limited to benzamide and benzoic acid derivatives such as procaine and procaine derivatives, utilized in compositions and methods for treating cortisol-mediated disorders, including but not limited to age-related depression, hypertension, Alzheimer's disease, and acquired immunodeficiency syndrome.

Abstract: The invention provides a therapeutic method for preventing or treating a pathological condition or symptom in a mammal, such as a human, wherein the infectivity of a pathogen such as a retrovirus toward mammalian cells is implicated and inhibition of its infectivity is desired comprising administering to a mammal in need of such therapy, an effective amount of an N-benzamide derivative of a piperazinyl amide of an amino acid thereof that inhibits pathogenic infectivity, including pharmaceutically acceptable salts thereof. The invention also provides a therapeutic method for preventing or treating a neuropathological condition or symptom in a mammal, such as human, comprising administering to a mammal in need of such therapy, an effective amount of an N-benzamide derivative of a piperazinyl amide of an amino acid thereof, including pharmaceutically acceptable salts thereof.

Abstract: The invention provides a therapeutic method for treating at least one symptom of a neurological disorder or disease such as Alzheimer's disease in a mammal, such as a human, wherein the toxicity of a pathogen of ? amyloid peptide and/or glutamate in mammalian cells is implicated and inhibition of the subsequently-induced pathological pathways is desired comprising administering to a mammal in need of such therapy, an effective amount of an N-arylamide or an (N-aminoalkyl)benzamide, including pharmaceutically acceptable salts thereof.

Abstract: The present invention relates to methods, kits, combinations, and compositions for treating, preventing or reducing the risk of developing a disorder or disease related to, or the symptoms associated with a neurodegenerative disorder such as neurotoxicity or a neuropathology in a subject, particularly to beta-amyloid-induced neurotoxicity and Alzheimer's disease. The invention further provides a method for inducing stem cell differentiation into neuronal cells, by administering to the patient a therapeutically effective amount of a compound of the invention.

Abstract: The present invention relates to the development of a pharmacological non-human animal model that associates memory loss to histopathological features found in the brain of a subject having Alzheimer's Disease. In one embodiment, a four-week continuous infusion of a Fe2+, A?42 and buthionine sulfoximine (FAB) solution in the left ventricle of young adult Long-Evans rats induced memory impairment accompanied by increased hyperphosphorylated Tau protein levels in cerebrospinal fluid. Brains from treated animals displayed neuritic plaques, tangles, neuronal loss, astrogliosis and microgliosis in hippocampus and cortex. The present invention may be utilized in evaluating preventive, therapeutic and diagnostic means for neurologic diseases.

Abstract: The present invention relates to methods, kits, combinations, and compositions for treating, preventing or reducing the risk of developing a disorder or disease related to, or the symptoms associated with, neurotoxicity in a subject, particularly to beta-amyloid-induced neurotoxicity and Alzheimer's disease. The compounds of the present invention are biologically active 22R-hydroxycholesterol derivatives containing a common spirost-5-en-3-ol structure.