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Mayo Clinic Technology
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Enodgenous Wild Type BRI Peptides as Potential Therapeutic Compound for the Treatment and Prevention of AD

Reference #:

2007-043

Inventors/Contributors

Todd E. Golde M.D., Yona R. Levites Ph.D., Craig W. Zwizinski Ph.D., Karen R. Jansen-West B.A., Victor M. Miller Ph.D., Jungsu Kim, Steven G. Younkin M.D., Ph.D., Fanggeng Zou Ph.D.

Description

Amyloid beta peptide (Abeta) accumulation within senile plaques, cerebral blood vessels walls, and diffuse immunoreactive deposits is a hallmark of Alzheimer’s disease (AD) pathology. The accumulation of aggregated Abeta is thought to initiate a pathological cascade that results in cognitive decline. Expression of an endogenous protein, BRI2, substantially inhibits Abeta accumulation in APP mice. This "anti-amyloidodgenic" effect appears to be attributable the release of a small 23 amino acid peptide sequence from the BRI2 precursor. Methods for producing and delivering the BRI23 wt and homologous peptides encoded by the RBI1 and BRI2 proteins and their use as AD therapeutics are claimed.

Patent Status

Pending

Contact

Susan L. Stoddard, Ph.D., Licensing Manager
sstoddard@mayo.edu

Mayo Foundation for Medical Education and Research
Office of Technology Commercialization
Centerplace 4
200 First Street SW
Rochester, MN 55905

Phone: (507) 284-1222
Fax: (507) 284-5410