Abstract: There is provided an assay for assessing the risk for developing substance dependency, including alcohol, opiate, cocaine, marijuana having a screening device for screening samples for the OPRM1+118A allele polymorphism, the presence of the allele indicating a risk of developing substance dependency. A method for diagnosing the risk for developing substance dependency by screening samples for the OPRM1+118A allele, whereby the presence of the allele indicates substance dependence is also provided. Also provided is a marker for determining the risk of developing substance dependency having an allele indicating the risk for developing substance dependency.

Abstract: The present invention provides methods and compositions for treating diseases and pathological conditions or processes mediated by undesired and/or uncontrolled angiogenesis (characterized as “angiogenic diseases”) by increasing the in vivo concentration of the A&bgr; peptide, or biologically active fragments or variants of the A&bgr; peptide, within a patient suffering from such diseases, conditions, or processes. The present invention also concerns diagnostic methods and kits for detection and measurement of anti-angiogenic A&bgr; peptide activity in biological fluids and tissues. Such diagnostic methods and kits can be utilized to screen compounds for potential therapeutic activity in the treatment of Alzheimer's disease.

Abstract: The subject invention provides methods of treating amyloidogenic diseases, comprising the administration of therapeutically effective amounts of a composition comprising a carrier and an agent that interferes with the interaction of CD40L and CD40R to an individual afflicted with an amyloidogenic disease. Also provided are methods and/or assay systems for the identification of compounds or other small molecules capable of disrupting the CD40R/CD40L signaling pathway.

Abstract: Methods for screening compounds for use in the treatment of neurodegenerative diseases such as Alzheimer's disease, multiple sclerosis, prion diseases, Huntington's disease, and Creutzfeldt-Jakob disease, where the screening methods include (a) measuring the vasoactivity of blood vessels when contacted sequentially with a &bgr;-amyloid peptide, phenylephrine, and a compound to be screened, and (b) measuring the inflammatory response, including cytokine release, when microglial cells are contacted with a &bgr;-amyloid peptide and then with a compound to be screened. The disclosed methods rely upon a common underlying mechanism for &bgr;-amyloid peptide-induced vasoactivity, &bgr;-amyloid peptide-induced inflammatory responses of microglial cells, and the pathogenesis of neurodegenerative diseases in general and Alzheimer's disease in particular, in which cGMP levels are increased by agents that counteract these three processes.

Abstract: CD45 isoform switching from the CD45RA to the CD45RO isoform is an indicator of peripheral CD4+ T lymphocyte function, as well as other blood cells. CD45 isoforms are altered on blood cells from AD patients compared to controls, showing significantly lower levels of CD45RA, and an increase in the CD45RO/CD45RA ratio compared to age-matched normal participants. The invention includes a method of assessing the risk of developing, of diagnosing, or of measuring the progression of Alzheimer's disease in a patient comprising of obtaining a blood sample from a patient, determining CD45 isoform expression of blood cells contained in the blood sample, and relating the determined CD45 isoform expression to an assessment of the risk of developing the disease, a diagnosis of the disease, or a measure of the progression of the disease. The blood cells, for purposes of illustration and not limitation, may comprise monocytes, macrophages, lymphocytes, or combinations thereof.

Abstract: A method of inhibiting the negative effects of beta-amyloid in the brain of an animal comprising administering an effective amount of a compound that modulates CD45 activity. This invention also relates to compositions for use in stimulating CD45, and assays for use in finding compounds useful in inhibiting the negative effects of beta-amyloid. An assay for use in identifying compounds that inhibit the negative effects of beta-amyloid comprises (a) contacting immune cells with a predetermined amount of one or more test compounds in the presence of beta-amyloid or one or more peptides derived therefrom, (b) monitoring the amount of one or more inflammatory molecules released by the immune cells, and (c) comparing the amount found in step (b) with another amount found in the absence of the one or more test compounds or using a different predetermined amount the one or more test compounds.

Abstract: There is provided a method and assay for detecting if a subject, especially subjects over the age of 79, is at increased risk of developing late onset Alzheimer's disease (AD) by directly or indirectly detecting polymorphisms in the cystatin C gene (CST3) in the subject, and observing whether or not the subject is at increased risk of developing late onset AD by determining the alleles present at an AD associated CST3 polymorphism, wherein the presence of particular alleles at the CST3 polymorphism indicates said subject is at increased risk of developing late onset AD.

Abstract: There is provided an assay for assessing the risk for developing substance dependency, including alcohol, opiate, cocaine, marijuana having a screening device for screening samples for the OPRM1+118A allele polymorphism, the presence of the allele indicating a risk of developing substance dependency. A method for diagnosing the risk for developing substance dependency by screening samples for the OPRM1+118A allele, whereby the presence of the allele indicates substance dependence is also provided. Also provided is a marker for determining the risk of developing substance dependency having an allele indicating the risk for developing substance dependency.

Abstract: A method is disclosed for treating and preventing diseases, wherein at least one of the causes of the disease is .beta.-amyloid peptide induced change in free radical production resulting in vascular endothelial dysfunction and vasoactivity, by antagonizing vascular free radicals in excess of functional equilibrium.

Abstract: A method is disclosed for treating and preventing diseases, wherein at least one of the causes of the disease is .beta.-amyloid peptide induced change in free radical production resulting in vascular endothelial dysfunction and vasoactivity, by antagonizing vascular free radicals in excess of functional equilibrium. An animal model for the disease is also disclosed.