Abstract: The present invention provides a method for decreasing cerebral vasoconstriction in a subject suffering from chronic or acute cerebral amyloid angiopathy which comprises administering to the subject an inhibitor of receptor for advanced glycation endproduct (RAGE) in an effective amount to inhibit transcytosis of amyloid &bgr; peptides across the blood-brain barrier in the subject, thereby decreasing cerebral vasoconstriction in the subject. The invention further provides for a method for ameliorating neurovascular stress in a subject which comprises administering to the subject an effective amount of an inhibitor of receptor for advanced glycation endproduct (RAGE), so as to increase cerebral blood flow in the subject, thereby ameliorating neurovascular stress in the subject.

Abstract: The present invention provides a method for decreasing cerebral vasoconstriction in a subject suffering from chronic or acute cerebral amyloid angiopathy which comprises administering to the subject an inhibitor of receptor for advanced glycation endproduct (RAGE) in an effective amount to inhibit transcytosis of amyloid &bgr; peptides across the blood-brain barrier in the subject, thereby decreasing cerebral vasoconstriction in the subject. The invention further provides for a method for ameliorating neurovascular stress in a subject which comprises administering to the subject an effective amount of an inhibitor of receptor for advanced glycation endproduct (RAGE), so as to increase cerebral blood flow in the subject, thereby ameliorating neurovascular stress in the subject.

Abstract: The invention provides for a non-human transgenic animal whose cells contain a recombinant DNA sequence comprising: (a) a nerve tissue specific promoter operatively linked to a DNA sequence which encodes human receptor for advanced glycation endproducts (RAGE), and (b) a nerve tissue specific promoter operatively linked to a DNA sequence encoding a mutant human amyloid precursor protein hAPP695, hAPP751 and hAPP770 bearing mutations linked to familial Alzheimer's disease in humans, wherein said non-human transgenic animal exhibits at least one phenotype from the group consisting of: increased expression of M-CSF gene in cerebral cortex; increased expression of IL-6 gene in cerebral cortex; increased neuronal stress; increased neurotoxicity; neuron loss; increased level of activated form of caspase 3 in brain; and increased level of phosphorylated tau protein in brain.

Abstract: The present method provides for an isolated peptide having an amino acid sequence corresponding to the amino acid sequence of a V-domain of a receptor for advanced glycation endproduct (RAGE). The present invention also provides for an isolated peptide having an amino acid sequence A-Q-N-I-T-A-R-I-G-E-P-L-V-L-K-C-K-G-A-P-K-K-P-P-Q-R-L-E-W-K (SEQ. ID No: 1). The present invention provides for a pharmaceutical composition comprising a therapeutically effect amount of an isolated peptide having an amino acid sequence corresponding to the amino acid sequence of a V-domain of RAGE.

Abstract: This invention provides a method for evaluating the ability of a compound to inhibit neurotoxicity which comprises (a) contacting a cell which expresses a receptor for advanced glycation end product protein and a mutant presenilin-2 protein in a cell culture and the compound; (b) determining the level of cell death in the cell culture; and (c) comparing the level of cell death determined in step (b) with the amount determined in the absence of the compound so as to evaluate the ability of the compound to inhibit neurotoxicity.

Abstract: The present invention provides a method for treating inflammation in a subject which comprises administering to the subject soluble receptor for advanced glycation endproduct (sRAGE) in an amount effective to inhibit binding of advanced glycation endproducts (AGEs) to RAGE thereby treating inflammation in the subject. The present invention also provides for a method for treating inflammation in a subject which comprises administering to the subject an agent in an amount effective to inhibit the interaction between receptor for advanced glycation endproduct (RAGE) and its ligand thereby treating inflammation in the subject.

Abstract: The present invention provides a method for decreasing cerebral vasoconstriction in a subject suffering from chronic or acute cerebral amyloid angiopathy which comprises administering to the subject an inhibitor of receptor for advanced glycation endproduct (RAGE) in an effective amount to inhibit transcytosis of amyloid &bgr; peptides across the blood-brain barrier in the subject, thereby decreasing cerebral vasoconstriction in the subject. The invention further provides for a method for ameliorating neurovascular stress in a subject which comprises administering to the subject an effective amount of an inhibitor of receptor for advanced glycation endproduct (RAGE), so as to increase cerebral blood flow in the subject, thereby ameliorating neurovascular stress in the subject.

Abstract: The present method provides for an isolated peptide having an amino acid sequence corresponding to the amino acid sequence of a V-domain of a receptor for advanced glycation endproduct (RAGE). The present invention also provides for an isolated peptide having an amino acid sequence A-Q-N-I-T-A-R-I-G-E-P-L-V-L-K-C-K-G-A-P-K-K-P-P-Q-R-L-E-W-K (Seq. I.D. No. 1). The present invention provides for a pharmaceutical composition comprising a therapeutically effect amount of an isolated peptide having an amino acid sequence corresponding to the amino acid sequence of a V-domain of RAGE.

Abstract: The present invention provides an isolated nucleic acid encoding an endoplasmic reticulum associated amyloid-beta peptide binding (ERAB) polypeptide. The ERAB polypeptide may comprise human ERAB polypeptide. The present invention provides a purified ERAB polypeptide, as well as a method for treating a neurodegenerative condition in a subject which comprises administering to the subject an agent in amount effective to inhibit ERAB polypeptide binding to amyloid-beta peptide so as to thereby treat the neurodegenerative condition.