New York University

Other

Jorge Ghiso

Blas Frangione

Thomas M Wisniewski

Einar M Sigurdsson

Miguel A Pappolla

Jin Ryoun Kim

Yang Hu

Ruben Vidal

Burkhard Poeggeler

Disclosed herein are methods for treating amyloid disease in humans by clearing amyloid peptides from one or more bodily fluids such as, e.g., blood, of a patient. In particular, the methods are based on the administration of compounds capable of binding to amyloid-beta (A&#x3b2;) or on dialysis of blood or plasma exchange in order to remove A&#x3b2; peptides from the blood circulation, and/or brain or other affected organs.

Method for treating amyloid disease

A peptide probe that generates fluorescence signals rapidly upon recognition of various A&#x3b2; aggregates without significant perturbation of samples. The present peptide probes display an increase in fluorescence signals upon coincubation with A&#x3b2; oligomers, but neither monomeric/dimeric species nor fibrils. The detection can occur within an hour or two without any additional sample preparation and incubation steps.

Peptide probe for rapid and specific detection of &#x3b2;-amyloid aggregation

Disclosed herein are methods for treating amyloid disease in humans by clearing amyloid peptides from one or more bodily fluids such as, e.g. blood, of a patient. In particular, the methods are based on the administration of compounds capable of binding to amyloid-beta (A&#x3b2;) or on dialysis of blood or plasma exchange in order to remove A&#x3b2; peptides from the blood circulation, and/or brain or other affected organs.

Two novel mutant amyloid protein precursors (ABriPP and ADanPP) and their amyloid peptides (ABri and ADan) associated with Familial British Dementia and Familial Danish Dementia, respectively, are disclosed. Genetic constructs comprising DNA encoding these proteins is used to produced transgenic mammals that are useful models for neurological diseases associated with amyloid deposits, neurofibrillary tangles, non-neuritic plaques, neuronal degeneration and behavioral deficits characteristic of dementia and other symptoms of the human diseases. These models are used for testing potential therapeutic agents and methods. Also provided is a DNA-based test for detecting the mutations, the mutant proteins and peptides, antibodies specific for the proteins and peptides. Immunoassays permit detection of the mutant proteins, particularly in affected brain tissue, or detection of an antibody specific for a mutant peptide.

Mutant genes in Familial British Dementia and Familial Danish Dementia

The cytotoxic effects of amyloid beta protein on cells are prevented by contacting the cells with an effective amount of an indole-3-propionic acid or a salt or ester thereof. Furthermore, a fibrillogenic disease can be treated in a human subject by administering to the human subject an amount of-an indole-3-propionic acid or a salt or ester thereof effective to prevent or reverse fibrillogenesis. Oxidation in a biological sample can be decreased by contacting the biological sample with an effective amount of an indole-3-propionic acid or a salt or ester thereof. Additionally, diseases or other conditions where free radicals and/or oxidative stress play a role can be treated by administering an effective amount of an indole-3-propionic acid or a salt or ester thereof.

Uses for indole-3-propionic acids and salts and esters thereof

The present invention relates to a method of using melatonin to reduce, inhibit or reverse the formation of amyloid fibrils and amyloid or amyloid-like deposits. The present invention also relates to a method for delaying the onset of Alzheimer's Disease or other amyloidosis-related diseases/disorders or for treating such diseases/disorders by administering an effective amount of melatonin to a subject in need thereof.

Growing community of inventors

Elmhurst, NY, United States of America

Jorge Ghiso