Abstract: Disclosed herein are methods for the quantification of ADDL binding to neuronal cells, including, but not limited to, primary cultures of hippocampal neurons. The method identifies and selects neurons based on any means capable of distinguishing neuronal cells, including, but not limited to, MAP2 immunoreactivity, which ensures that glial cells are excluded from an ADDL binding analysis; antibodies selective for neuronal cell surface receptors and/or other surface markers; reagents specific for neuronal signalling markers present intracellularly; and the like. Furthermore, ADDL binding occurs in a sub-population of 16 DIV neurons and is heterogeneous in intensity among individual cells. Also, ADDL binding can be further specified and quantified by using additional markers. Additionally, the presence or absence of ADDL binding is used to identify, characterize, analyze, assess, and/or evaluate agents (e.g.

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: Disclosed herein are antibodies that bind with high specificity to soluble oligomers of amyloid ? (Abeta) and methods of employing those antibodies. The antibodies are able to distinguish between Alzheimer's Disease (AD) and control human brain extracts. The antibodies identify endogenous Abeta oligomers in AD brain slices and also bind to Abeta oligomers on cultured hippocampal cells. The antibodies neutralize endogenous Abeta oligomers and Abeta oligomers produced in solution.

Abstract: The present invention provides amyloid ? peptide assemblies composed of at least three amyloid ? peptide subunits, wherein at least one of the amyloid ? peptide subunits is an amyloid ? peptide analog. The invention further relates to metal complexes of amyloid ? peptide assemblies and the use of amyloid ? peptide assemblies as vaccines and in the identification of agents that modulate assembly of the amyloid ? peptide subunits.

Abstract: The invention herein comprises antibodies that bind to amyloid beta-derived diffusible ligands (ADDLs). ADDLs comprise amyloid ? protein assembled into soluble, globular, non-fibrillar, oligomeric structures capable of activating specific cellular processes.

Abstract: The invention provides amyloid beta-derived dementing ligands (ADDLs) that comprise amyloid ? protein assembled into globular non-fibrillar oligomeric structures capable of activating specific cellular processes. The invention also provides methods for assaying the formation, presence, receptor protein binding and cellular activity of ADDLs, as well as compounds that block the formation or activity of ADDLs, and methods of identifying such compounds. The invention further provides methods of using ADDLs, and modulating ADDL formation and/or activity, inter alia in the treatment of learning and/or memory disorders.

Abstract: The invention described in this disclosure involves a new composition of matter, amyloid beta-derived dementing ligands (ADDL's). ADDLs consist of amyloid ? peptide assembled into soluble globular non-fibrillar oligomeric structures that are capable of activating specific cellular processes. The invention further encompasses methods for assaying the formation, presence, receptor protein binding and cellular activities of ADDLs. The invention further encompasses assay methods and inhibitor molecules for cellular signaling molecules activated by ADDLs. Also described are molecules that block proteins that promote the formation of ADDLs.

Abstract: The present invention relates to C34 peptide derivatives that are inhibitors of viral infection and/or exhibit antifusogenic properties. In particular, this invention relates to C34 derivatives having inhibiting activity against human immunodeficiency virus (HIV), respiratory syncytial virus (RSV), human parainfluenza virus (HPV), measles virus (MeV), and simian immunodeficiency virus (SIV) with long duration of action for the treatment of the respective viral infections.

Abstract: The present invention provides compositions and methods for the treatment or prevention of Alzheimer's disease. More particularly, the invention provides a combination therapy for the treatment or prevention of Alzheimer's disease, wherein the therapy comprises administering to a subject an amyloid beta vaccine in combination with a cyclooxygenase-2 selective inhibitor.

Abstract: The present invention provides for use of bupropion or a pharmaceutically acceptable salt thereof in the treatment of restless legs syndrome in humans.

Abstract: The invention herein comprises antibodies that bind to amyloid beta-derived diffusible ligands (ADDLs). ADDLs comprise amyloid &bgr; protein assembled into soluble, globular, non-fibrillar, oligomeric structures capable of activating specific cellular processes. The invention also comprises methods of using ADDL-specific antibodies for assaying the formation, presence, receptor protein binding and cellular activity of ADDLs, as well as using such antibodies to detect compounds that block the formation or activity of ADDLs, and methods of identifying such compounds. The invention further provides methods of using ADDL-specific antibodies in modulating ADDL formation and/or activity, inter alia in the treatment of learning and/or memory disorders.

Abstract: The invention described in this disclosure involves a new composition of matter, amyloid beta-derived dementing ligands (ADDL's). ADDLs consist of amyloid &bgr; peptide assembled into soluble globular non-fibrillar oligomeric structures that are capable of activating specific cellular processes. The invention further encompasses methods for assaying the formation, presence, receptor protein binding and cellular activities of ADDLs. The invention further encompasses assay methods and inhibitor molecules for cellular signaling molecules activated by ADDLs. Also described are molecules that block proteins that promote the formation of ADDLs.

Abstract: This invention relates to genetically engineered enzymes, their ligand conjugates, their manufacture, and their use in qualitative or quantitative assays. A hybrid enzyme, such as an AP-epitope, has a foreign amino acid moiety (an epitope) inserted near the active site of the starting AP enzyme. The foreign amino acid moiety binds with an analyte, and, as a consequence of this binding, the enzymatic activity of the hybrid enzyme, AP-epitope, is modified. The changes in the enzymatic activity are dependent upon the presence, or the amount, of the analyte. In another embodiment, the hybrid enzyme consists of a cysteine introduced near the active site of an AP to give a hybrid enzyme. The cysteine on the hybrid enzyme serves as a point of conjugation of a ligand, such as theophylline, ferritin, thyroxine, or digoxigenin, to form the hybrid enzyme-ligand conjugate.