Madhusudhanan Narasimhan has completed his PhD at the age of 26 years from Madras University, India and postdoctoral studies from Nova Southeastern University, Florida, USA and UTHSCSA, San Antonio, Texas, USA. He is currently working as a Senior Research Associate in Dept. of Pharmacology and Neuroscience, TTUHSC, Lubbock, Texas. He has published more than 15 papers in reputed journals and serving in Editorial Board and as reviewer for toxicology and pharmacology journals of repute.


Injuries in fetal rat cortical neurons associated with Fetal Alcohol Syndrome are correlated to ethanol exposure leading to increased oxidative stress, GSH depletion, and ultimately neuroapoptosis. Previous finding from our laboratory demonstrated that over expression of Nrf2, a redox-sensitive transcription factor that controls antioxidant homeostasis thus preventing ethanol induced oxidative stress and degeneration of neurons (Narasimhan et al., 2011). In general, astrocytes have high basal Nrf2 levels thus affording protection to neurons against various insults. As neuron survival and function are intimately connected to glia with which neurons are commingled, the early prenatal brain development is very critical where the role of glia/astrocytes is either none or minimal. Though degradation based regulation of Nrf2 is reported during early developmental period, the role of microRNA (miRNA) associated post-transcriptional regulation is less understood. Bioinformatics search predicted 408 plausible miRNAs that could target human NFE2L2 protein and herein we have validated a group of four miRNAs targeting Nrf2 in neuronal cells. Further over expression of these miRNAs has been identified to target Nrf2 dependent antioxidant response (ARE)/GSH. Our group has demonstrated that alcohol could negatively alter GSH homeostasis causing neuro-degeneration. Currently, studies are underway to test the role of these miRNAs in alcohol induced Nrf2 based oxidative stress/GSH pathway