Investigating the Annexin A1-Formyl Peptide Receptor Pathway to Develop Innovative Anti-stroke Drugs
Stroke is the third leading cause of death in the USA, and despite this high mortality, 76% of those having strokes survive, often with moderate or severe disabilities. One of the key therapeutic approaches targets thrombus- the blood clot that occludes the blood vessel. At present, the thrombolytic drug, tissue plasminogen activator (tPA), constitutes the only FDA-approved therapy for acute ischemic stroke. However, the therapeutic window is limited to 3-6 hours from stroke onset, which, combined with haemorrhagic complications, means only 2-3% of US patients receive treatment. Although the exact mechanism(s) responsible for the brain damage occurring after an ischemic insult is/are not fully understood, there is an increasing amount of evidence suggesting that post-ischemia inflammation is a significant contributing factor to the pathogenic process. We, and others, have shed some light on biochemical pathways centered on endogenous inhibitors endowed with counter-regulatory and protective functions. One such biochemical pathway, and potential therapeutic strategy for the treatment of stroke, is the novel target: the Annexin A1-Formyl Peptide Receptor Pathway (or AnxA1-FPR pathway). Whilst our previous data have demonstrated that AnxA1 targets vascular and parenchyma phenomena (via an FPR pathway), little is known about what happens in deep brain structures such as deep cortical layers and the underlying striatum. This project aims to address this lack of knowledge, in order to fully validate this novel target as a potential therapeutic for stroke, and possible other neurovascular diseases.
Principal Investigator: Murray, Teresa -- Biomedical Engineering/CBERS
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