Novel Methods for Reducing Inflammation and Treating Diseases such as Parkinson?s and Alzheimer?s Disease
Posted Jun 13 2010 5:00pm
Description of Invention: Activated microglia mediate inflammation in the CNS by secreting various cytokines and free radicals that could damage neurons. Brains from patients with Parkinson disease show microglia reaction, and previous studies by this laboratory show microglia activation leads to inflammation mediated dopaminergic degeneration. Thus identification of drugs that reduce microglia activation could prevent or reverse neuronal degeneration in Parkinson’s Disease, Alzheimer’s Disease, ischemia and other degenerative CNS disorders.
Considerable research has shown the ability of various peptides to attenuate microglia activation and prevent neuronal degeneration in vitro with a bi-modal dose response curve. These peptides demonstrate maximum effects at femto-molar and micro-molar concentrations. These inventors have now discovered small-peptide and non-peptide molecules that also inhibit microglia and prevent neuronal degeneration with the same bi-modal dose response curve. The non-peptide compounds have also been shown to prevent dopamine neuronal degeneration in animal models. The present invention provides compositions and methods for inhibiting inflammatory mechanisms and treating inflammation-related condition by administering ultra-low (femto-molar) doses of at least one compound of the invention. These compounds include morphinans, opioid peptides, and the tripeptide GGF.
Licensing Status: In addition to licensing, the technology is available for further development through collaborative research with the inventors via a Cooperative Research and Development Agreement (CRADA).
Portfolios: Internal Medicine Internal Medicine - Therapeutics Central Nervous System Central Nervous System - Therapeutics In-vitro 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: email@example.com Phone: 301-435-5502 Fax: 301-402-0220