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Agents Useful for Reducing Amyloid Precursor Protein and Treating Dementia and Methods of Use Thereof

Posted Jun 14 2010 5:00pm

Description of Invention:
Alzheimer's disease (AD) is a progressive neurodegenerative condition leading to loss of memory and other cognitive functions. Alzheimer's disease is characterized pathologically by the appearance of senile plaques, primarily composed of amyloid b protein (Ab), and neurofibrillary tangles in the CNS. Treatments reducing potentially toxic Ab may thus prevent the occurrence and progression of Alzheimer's disease. As Ab is derived from the larger b amyloid precursor protein (bAPP), reducing the production of bAPP should provide a therapy for the treatment of Alzheimer's disease.

The production of bAPP is regulated by cytokines, muscarinic receptors, and some cholinesterase inhibitors. The latter also have some utility in treating the symptoms of Alzheimer's disease. The agents and methods disclosed and claimed in this patent application reduce the production of bAPP and Ab in vivo and in vitro without cholinergic side effects or other toxicity. The agents are structurally related to a known anti-cholinesterase agent in current clinical assessment, but are devoid of anticholinesterase activity and associated side effects. They likely act on a recently described translational regulatory element on bAPP mRNA. Further information as to how these agents effect bAPP processing can be found in the Proceedings of the National Academy of Sciences, Volume 98(13), Pages 7605-7610, June 19, 2001.



Inventors:
Nigel H Greig (NIA)


Patent Status:
HHS, Reference No. E-141-2000/0
US, , Patent No. 7,153,882, Issued 26 Dec 2006
US, Application No. 11/455,959 filed 20 Jun 2006



Portfolios:
Central Nervous System
Central Nervous System - Therapeutics
In-vivo Data



For Additional Information Please Contact:
Norbert Pontzer Ph.D., J.D.
NIH Office of Technology Transfer
6011 Executive Blvd. Suite 325 Room 23,
Rockville, MD 20852
United States
Email: pontzern@mail.nih.gov
Phone: 301-435-5502
Fax: 301-402-0220


Ref No: 501

Updated: 06/2010

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