Position title: Professor of Neurological surgery and Vice Chair for Research
My research is to decipher the molecular mechanisms of post-stroke brain damage and to test novel therapies. My particular interest is to evaluate the interactive role of noncoding RNAs (ncRNAs), transcription factors and epigenetic modifications in modulating the pathophysiologic events that promote secondary brain damage. Comorbid conditions like diabetes and hypertension increase the vulnerability to stroke. Thus, we use type-2 diabetic animal models in some experiments to better understand the mechanisms by which diabetes promotes post-stroke brain damage. Additionally, we have found that preconditioning promotes ischemic tolerance that decreases the negative impact leading to better recovery in case of an unavoidable stroke. My lab is evaluating the modalities and mechanisms that promote ischemic tolerance. We have found that intermittent fasting elicits altered epigenetic and transcriptional programming leading to reduced oxidative stress, inflammation, mitochondrial damage and cell death. Thus, intermittent fasting is a potential dietary intervention to not only mitigate metabolic disorders like diabetes and hypertension, but to also decrease the occurrence of devastating age-related diseases like heart attack, stroke and dementia.