Novel Tissue Protector for Subarachnoid Hemorrhage

Award Information
Agency: Department of Health and Human Services
Branch: N/A
Contract: 1R41NS054319-01
Agency Tracking Number: NS054319
Amount: $171,707.00
Phase: Phase I
Program: STTR
Awards Year: 2005
Solicitation Year: N/A
Solicitation Topic Code: N/A
Solicitation Number: N/A
Small Business Information
Cognosci, Inc.
Cognosci, Inc., Box 12076, 2 Davis Dr, Research Triangle Park, NC, 27709
HUBZone Owned: N
Woman Owned: N
Socially and Economically Disadvantaged: N
Principal Investigator
 (919) 765-0028
Business Contact
Phone: (919) 765-0028
Research Institution
 2424 Erwin Rd.
Suite 1103
DURHAM, NC, 27705
 Nonprofit college or university
DESCRIPTION (provided by applicant): There are approximately 30,000 new cases of aneurysmal subarachnoid hemorrhage (SAH) in this country, making it a significant health care problem. Despite advances in the medical and surgical care of patients with SAH, this condition still has a high morbidity and mortality, with a 30 day mortality of nearly 50%. In order to examine the pathophysiology of vasospasm following SAH and to take advantage of transgenic technology, we recently characterized a murine model of SAH. This model is an extension of the standard monofilament middle cerebral artery occlusion (MCAO) model performed in our lab and by others around the world (Parra et al. 2002). Using this model, we now demonstrate that animals expressing the epsilon 4 isoform of apolipoprotein-E (apoE4) are significantly more impaired on behavioral tests following SAH than their apoES counterparts. This situation is similar to Alzheimer's disease where patients expressing apoE4 are significantly more impaired and have an earlier age of onset than their apoES counterparts. Cognosci has developed novel mimetic peptides of apoE holo-protein which appear to retain the anti-inflammatory and neuroprotective properties of apoE holo-protein. In pilot studies, we show that 1 of these peptides, COG1410, can significantly improve survival when administered following SAH, compared to animals receiving SAH and saline vehicle as a control. Based on these pilot studies, we now wish to fully test the ability of apoE peptide mimetics to inhibit the behavioral and vasospastic deficits that follow experimental application of subarachnoid hemorrhage in a mouse model.

* information listed above is at the time of submission.

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