Ischemic stroke is a leading cause of disability and death in the United States with over half a million people being afflicted each year. Stroke patients often face high healthcare costs and a significant reduction in their quality of life. The stroke pathophysiology is driven by complex molecular mechanisms that are not yet fully understood, which has, in part, hampered the development of effective therapeutic interventions for stroke patients. Our goal is to enhance our knowledge of the early molecular processes that drive subsequent cellular and tissue-level changes that result in brain damage and neurological dysfunction so that we may harness this information to develop new treatments against stroke. On this front, our research is focused on the noncoding genome and, particularly, on the roles and functions of neural noncoding RNAs (ncRNAs) that show specific and robust responses to the stroke injury and participate in post-stroke gene regulation. We are studying how the interplay between ncRNAs, regulatory proteins and DNA drives the gene regulatory networks that underlie the development of the post-stroke pathophysiology. Because RNAs are fairly easily amenable to therapeutic manipulations, we hope to discover new druggable targets that can be further researched and developed for preclinical and clinical applications against stroke.

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A snapshot of ischemic stroke

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