Cathepsin d is an amyloidogenic protease in alzheimer's disease

Details Cathepsin d is an amyloidogenic protease in alzheimer's disease Cathepsin d is an amyloidogenic protease in alzheimer's disease

A - Human Necessities

61

K

A61K 38/55 (2006.01) A61K 31/215 (2006.01) A61K 31/41 (2006.01) A61K 31/44 (2006.01) A61K 31/445 (2006.01) A61K 31/535 (2006.01) A61K 38/05 (2006.01) A61K 38/06 (2006.01) A61K 38/07 (2006.01) A61K 45/00 (2006.01) C12N 9/48 (2006.01) C12N 9/99 (2006.01) C12Q 1/00 (2006.01) C12Q 1/37 (2006.01) G01N 33/53 (2006.01) G01N 33/549 (2006.01) G01N 33/573 (2006.01) C07D 211/38 (2006.01) C07D 261/02 (2006.01) C07D 409/12 (2006.01) C07D 409/14 (2006.01) C07K 5/03 (2006.01)

Patent

CA 2175564

Deposition of the neurotoxic beta-amyloid peptide is a pathologic process that takes place in the brains of Alzheimer's disease patients. Disclosed are methods for treating a patient with a therapeutic compound that functions by blocking the formation of beta-amyloid from the amyloid precursor protein (APP). We have identified the aspartic protease cathepsin D as a protease responsible for amyloidogenic processing of APP. Non-toxic compounds are disclosed that block both the in vitro activity of human cathepsin D, and the release of beta-amyloid by human cells. Such aspartic protease inhibitors thus have utility as therapeutics for Alzheimer's disease by blocking the pathologic accumulation of beta-amyloid.

Le dépôt du peptide bêta-amyloïde neurotoxique est un processus pathologique qui se déroule dans le cerveau de patients atteints de la maladie d'Alzheimer. L'invention se rapporte à des procédés qui consistent à traiter un patient avec un composé thérapeutique qui agit en bloquant la formation de la bêta-amyloïde issue de la protéine précurseur d'amyloïde (APP). Nous avons identifié la protéase aspartique cathepsine D comme étant une protéase responsable de la transformation amyloïdogène de l'APP. L'invention se rapporte également à des composés non toxiques qui bloquent à la fois l'activité in vitro de la cathepsine D humaine, et la libération de la béta-amyloïde par les cellules humaines. Ces inhibiteurs de la protéase aspartique sont donc utiles comme agents thérapeutiques pour traiter la maladie d'Alzheimer en bloquant l'accumulation pathologique de bêta-amyloïde.

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