Abstract: A method of diagnosing Alzheimer's disease in a patient comprises determining whether the phosphorylation level of an indicator protein in cells of the patient after stimulus with an activator compound is abnormally elevated as compared to a basal phosphorylation level, the indicator protein being e.g. Erk1/2 and the activator compound being e.g. bradykinin.

Abstract: This invention is a method and kit for treating a disease associated with, or resulting from, the accumulation of soluble oligomer amyloid beta 1-42 using an antibody, or antibody fragment thereof, that has a higher affinity for amyloid beta 1-42 oligomers than for amyloid beta 1-42 monomer, amyloid beta 1-40 monomer, plaques and amyloid beta fibrils and, optionally, a tau therapeutic or an inhibitor of amyloid beta production or aggregation.

Abstract: The present invention relates to antibodies that bind amyloid ?-derived diffusible ligands, also known as ADDLs. The antibodies of the invention are selective for ADDLs, can penetrate the brain, and are useful in methods of detecting ADDLs and diagnosing Alzheimer's disease. The present antibodies also block binding of ADDLs to neurons, assembly of ADDLS, and tau phosphorylation and are there useful in methods for the preventing and treating diseases associated with ADDLs.

Abstract: This invention is a selective A? oligomer kit and immunoassay method capable of reliably and sensitively detecting A? oligomers in a biological sample of a patient. In one embodiment the inventive assay uses a pair of anti-A? oligomer antibodies, as capture and detection antibodies, to detect and quantify A? oligomers. The method can be used to differentiate Alzheimer's disease (AD) patients from non-AD patients and/or to stratify AD patients according to the severity of their disease.

Abstract: A method of diagnosing Alzheimer's disease in a patient comprises determining whether the phosphorylation level of an indicator protein in cells of the patient after stimulus with an activator compound is abnormally elevated as compared to a basal phosphorylation level, the indicator protein being e.g. Erk1/2 and the activator compound being e.g. bradykinin.

Abstract: This invention is a method and kit for treating a disease associated with, or resulting from, the accumulation of soluble oligomer amyloid beta 1-42 using an antibody, or antibody fragment thereof, that has a higher affinity for amyloid beta 1-42 oligomers than for amyloid beta 1-42 monomer, amyloid beta 1-40 monomer, plaques and amyloid beta fibrils, wherein the antibody is in combination with a tau therapeutic or an inhibitor of amyloid beta production or aggregation.

Abstract: This invention is a selective A? oligomer kit and immunoassay method capable of reliably and sensitively detecting A? oligomers in a biological sample of a patient. In one embodiment the inventive assay uses a pair of anti-A? oligomer antibodies, as capture and detection antibodies, to detect and quantify A? oligomers. The method can be used to differentiate Alzheimer's disease (AD) patients from non-AD patients and/or to stratify AD patients according to the severity of their disease.

Abstract: This invention is a selective A? oligomer kit and immunoassay method capable of reliably and sensitively detecting A? oligomers in a biological sample of a patient. In one embodiment the inventive assay uses a pair of anti-A? oligomer antibodies, as capture and detection antibodies, to detect and quantify A? oligomers. The method can be used to differentiate Alzheimer's disease (AD) patients from non-AD patients and/or to stratify AD patients according to the severity of their disease.

Abstract: The present invention relates to antibodies that bind amyloid ?-derived diffusible ligands, also known as ADDLs. The antibodies of the invention are selective for ADDLs, can penetrate the brain, and are useful in methods of detecting ADDLs and diagnosing Alzheimer's disease. The present antibodies also block binding of ADDLs to neurons, assembly of ADDLS, and tau phosphorylation and are there useful in methods for the preventing and treating diseases associated with ADDLs.

Abstract: The invention herein is directed to immunoassays for the detection of A?42 oligomers. The inventive assays are based on the observations herein that the presence of A?42 oligomers in a preparation is directly related to a decrease in a C-terminal (CT) immunosignal and a correlated increase in an N-terminal (NT) immunosignal, relative to the immunosignal generated in the absence of A?42 oligomers, in an A?42 CT and NT ELISA assay and an A?42 CT AlphaLISA assay. The invention herein involves the use of these assays alone or in combination to screen for inhibitors of A?42 oligomerization.

Abstract: This invention relates to methods of diagnosing Alzheimer's disease and methods of screening for compounds for the treatment or prevention of Alzheimer's disease. The methods are based upon newly discovered differences in protein phosphatase 2A (PP2A) function and related molecular events in Alzheimer's disease cells compared to control cells. In one embodiment, differences in basal PP2A gene expression in Alzheimer's cells are compared to controls. In another embodiment differences in PP2A protein and enzyme activity are compared in test and control cells. In another embodiment differences in response to substances that inhibit PP2A function are compared. Still another embodiment detects differences in the subcellular distribution of phosphorylated Erk1/2, a substrate of PP2A, in normal and Alzheimer's disease cells.

Abstract: Disclosed are antibodies that bind amyloid beta-derived diffusible ligands, also known as ADDLs. The antibodies are selective for ADDLs, can penetrate the brain, and are useful in methods of detecting ADDLs and diagnosing Alzheimer's disease. The antibodies also block binding of ADDLs to neurons, assembly of ADDLS, and tau phosphorylation and are there useful in methods for the preventing and treating diseases associated with ADDLs.

Abstract: The present invention relates to methods for enhancing the cellular uptake and clearance of soluble oligomeric A? peptide assemblies from the environment surrounding both neuronal and non-neuronal cells. Oligomeric A? peptide assembly uptake and clearance is achieved via an agent that enhances insulin receptor signaling. Such ADDL uptake enhancers represent effective anti-ADDL therapeutics for use in the therapeutic treatment and/or prophylactic treatment of diseases including Alzheimer's disease, Down's syndrome, and the like, in which compromised nerve cell function is linked to the formation and/or the activity of soluble oligomeric A? peptide assemblies, also known as ADDLs, and ADDL-related assemblies.

Abstract: A method of diagnosing Alzheimer's disease in a patient comprises determining whether the phosphorylation level of an indicator protein in cells of the patient after stimulus with an activator compound is abnormally elevated as compared to a basal phosphorylation level, the indicator protein being e.g. Erk1/2 and the activator compound being e.g. bradykinin.

Abstract: A method of diagnosing Alzheimer's disease in a patient comprises determining whether the phosphorylation level of an indicator protein in cells of the patient after stimulus with an activator compound is abnormally elevated as compared to a basal phosphorylation level, the indicator protein being e.g. Erk1/2 and the activator compound being e.g. bradykinin.

Abstract: This invention relates to methods of diagnosing Alzheimer's disease and methods of screening for compounds for the treatment or prevention of Alzheimer's disease. The methods are based upon newly discovered differences in protein phosphatase 2A (PP2A) function and related molecular events in Alzheimer's disease cells compared to control cells. In one embodiment, differences in basal PP2A gene expression in Alzheimer's cells are compared to controls. In another embodiment differences in PP2A protein and enzyme activity are compared in test and control cells. In another embodiment differences in response to substances that inhibit PP2A function are compared. Still another embodiment detects differences in the subcellular distribution of phosphorylated Erk1/2, a substrate of PP2A, in normal and Alzheimer's disease cells.

Abstract: The present invention relates to methods for enhancing the cellular uptake and clearance of soluble oligomeric A? peptide assemblies from the environment surrounding both neuronal and non-neuronal cells. Oligomeric A? peptide assembly uptake and clearance is achieved via an agent that enhances insulin receptor signaling. Such ADDL uptake enhancers represent effective anti-ADDL therapeutics for use in the therapeutic treatment and/or prophylactic treatment of diseases including Alzheimer's disease, Down's syndrome, and the like, in which compromised nerve cell function is linked to the formation and/or the activity of soluble oligomeric A? peptide assemblies, also known as ADDLs, and ADDL-related assemblies.

Abstract: A method of diagnosing Alzheimer's disease in a patient comprises determining whether the phosphorylation level of an indicator protein in cells of the patient after stimulus with an activator compound is abnormally elevated as compared to a basal phosphorylation level, the indicator protein being e.g. Erk1/2 and the activator compound being e.g. bradykinin.

Abstract: The invention provides a method for modulating attentive cognition comprising administering a compound that alters intraneuronal carbonic anhydrase activity thereby affecting establishment of a theta rhythm. The metabolic pathway of the compound preferably involves bicarbonate-mediated GABAergic depolarization. The term “attentive cognition” is meant to encompass memory formation, learning, spatial memory, and attention. The modulating may be stimulating, or the compound may have the multiple effects of inhibiting intraneuronal carbonic anhydrase activity, establishment of a theta rhythm, and memory acquisition. The invention further provides a method of modulating memory and attention comprising switching theta rhythm on and off, the switching comprising potentiating or inhibiting intraneuronal carbonic anhydrase activity.

Abstract: The invention provides a method for modulating attentive cognition comprising administering a compound that alters intraneuronal carbonic anhydrase activity thereby affecting establishment of a theta rhythm. The metabolic pathway of the compound preferably involves bicarbonate-mediated GABAergic depolarization. The term “attentive cognition” is meant to encompass memory formation, learning, spatial memory, and attention. The modulating may be stimulating, or the compound may have the multiple effects of inhibiting intraneuronal carbonic anhydrase activity, establishment of a theta rhythm, and memory acquisition. The invention further provides a method of modulating memory and attention comprising switching theta rhythm on and off, the switching comprising potentiating or inhibiting intraneuronal carbonic anhydrase activity.