Abstract: In vivo and in vitro methods of increasing amyloid deposition using amyloid-enhancing compounds are described. Methods of forming amyloid fibrils and screening for agents useful in treating amyloidosis are also described. Animals having non-naturally occurring amyloid deposits produced using the amyloid-enhancing compounds even further are described.

Abstract: Therapeutic compounds and methods for inhibiting amyloid deposition in a subject, whatever its clinical setting, are described. Amyloid deposition is inhibited by the administration to a subject of an effective amount of a therapeutic compound comprising an anionic group and a carrier molecule, or a pharmaceutically acceptable salt thereof, such that an interaction between an amyloidogenic protein and a basement membrane constituent is inhibited. Preferred anionic groups are sulfonates and sulfates. Preferred carrier molecules include carbohydrates, polymers, peptides, peptide derivatives, aliphatic groups, alicyclic groups, heterocyclic groups, aromatic groups and combinations thereof.

Abstract: Therapeutic compounds and methods for inhibiting amyloid deposition in a subject, whatever its clinical setting, are described. Amyloid deposition is inhibited by the administration to a subject of an effective amount of a therapeutic compound comprising an anionic group and a carrier molecule, or a pharmaceutically acceptable salt thereof, such that an interaction between an amyloidogenic protein and a basement membrane constituent is inhibited. Preferred anionic groups are sulfonates and sulfates. Preferred carrier molecules include carbohydrates, polymers, peptides, peptide derivatives, aliphatic groups, alicyclic groups, heterocyclic groups, aromatic groups and combinations thereof.

Abstract: Therapeutic compounds and methods for inhibiting amyloid deposition in a subject, whatever its clinical setting, are described. Amyloid deposition is inhibited by the administration to a subject of an effective amount of a therapeutic compound comprising an anionic group and a carrier molecule, or a pharmaceutically acceptable salt thereof, such that an interaction between an amyloidogenic protein and a basement membrane constituent is inhibited. Preferred anionic groups are sulfonates and sulfates. Preferred carrier molecules include carbohydrates, polymers, peptides, peptide derivatives, aliphatic groups, alicyclic groups, heterocyclic groups, aromatic groups and combinations thereof.

Abstract: A method for identifying compounds useful for treating patients with amyloidosis is disclosed. Compounds are screened according to the present invention to determine their ability to modulate the affinity between amyloid protein and proteins of the extracellular matrix.

Abstract: L-sucrose or .beta.-L-fructofuranosyl .alpha.-L-glucopyranoside--(I), the enantiomer of naturally occuring D-sucrose, which does not appear in nature has been synthesized and has been found to be sweet. It is unlikely that L-sucrose is metabolized in the manner of D-sucrose. In a preferred process for producing L-sucrose the key step is the condensation of 2,3,4,6-tetra-O-benzyl-.alpha.-L-glucopyranosyl chloride--(II) with 1,3,4,6-tetra-O-benzyl-L-fructofuranose--(III). Compound II is obtained from L-glucose by way of 2,3,4,6-tetra-O-benzyl-.alpha.-L-glucopyranose; and L-glucose is prepared from L-arabinose by nitromethane synthesis. Compound III is obtained by oxidation, with Jones reagent, of 1,3,4,6-tetra-O-benzyl-L-mannitol which, in turn, is prepared from L-mannose. The condensation product of II and III is catalytically debenzylated to produce L-sucrose.