BME PhD Prospectus Defense - Smrithi Sunil

  • Starts: 10:00 am on Monday, December 10, 2018

Title: “The evolution of neurovascular coupling during stroke recovery”

Committee: David Boas, PhD – BU BME/ECE (Advisor, Chair) Xue Han, PhD – BU BME Kıvılcım Kılıç, MD/PhD – BU BME Anna Devor, PhD – UCSD Neuroscience and Radiology Cenk Ayata, MD – MGH/HMS Stroke, Neurology, and Radiology

Abstract: Stroke is the leading cause of long-term disability worldwide and approximately 795,000 people experience a stroke each year in the United States alone. Cellular and vascular impairments are complex and highly integrative mechanisms that begin within a few minutes after stroke and lead to tissue damage and ultimately the loss of sensory and motor function. Some spontaneous behavioral recovery is usually seen in the weeks to months following stroke in human patients and imaging hemodynamics using functional magnetic resonance imaging (fMRI) is widely used to study the basis of behavioral recovery from stroke. fMRI studies in patients show significant plasticity in the brain, occurring in areas surrounding the lesion as well as distant regions such as homologous regions in the contralesional (unaffected) hemisphere. However, it is incompletely understood to what extent a change in the vasculature or the neuronal activity results in the observed changes in the fMRI hemodynamic signals. Understanding the changes to the underlying brain activity and vasculature following a stroke will aid in better interpretation of the fMRI signal in human patients and guide better rehabilitation or other therapeutic approaches to enhance recovery. To this end, the main goal of this project is to study the evolution of neurovascular coupling in a chronic mouse model to understand the underlying contributions of neuronal activity and vasculature during stroke recovery. We also propose an acute therapeutic approach to enhance functional recovery after stroke. In Aim 1 we will optimize a mouse photothrombotic stroke model and characterize the spatiotemporal evolution of blood flow and vascular structure. In Aim 2 we will correlate the hemodynamic signals to neural activity and determine the contributions of excitatory and inhibitory cells to the hemodynamic signals during stroke recovery. Finally, in Aim 3 we propose an acute therapy to enhance functional recover after stroke.

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