Email: ariar@bwh.harvard.edu
Research Interests: Fetal Alcohol Syndrome
Amyotrophic Lateral Sclerosis (ALS)
Neurosciences
Cancer Biology
Environmental toxicology
Neurobiology
Neurogenesis
Cerebral cortex
Mitochondrial biology
Unfolded protein response
Substance Abuse
Protein misfolding
Signal transduction
Gene expression
Cell cycle
Mucosal immunology
Biography: I joined Brigham and Women’s Hospital (BWH), Harvard affiliated hospital as a Research Manager in the Department of Medicine in 2016. Prior to coming to BWH, I worked as a Senior Research Associate at Mount Sinai School of Medicine, New York. I received B.S in Pharmacy from India and Ph.D. and MBA from Texas Tech University Health Sciences Center, Texas, USA.
During my doctoral training, my research project was focused on exploring the molecular mechanisms underlying abnormal neurogenesis in fetal alcohol syndrome. I investigated the effect of ethanol on Tbr2-positive basal progenitor cell proliferation which populate the cortical layers and conversely the mechanism of alcohol-induced cerebral cortex abnormalities resulting from impaired proliferation. I have shown that ethanol inhibits the proliferation of basal progenitors through altering the expression of cell cycle proteins. My studiesalso revealed that ethanol alters the activity of glycogen synthase kinase 3? (GSK-3?) signaling pathway in central nervous system, where it is predominantly found and modifies various neurogenetic processes by regulating downstream targets.
My postdoctoral research involved understanding the role of mitochondrial unfolded protein response (UPR) in SOD1-G93A model of amyotrophic lateral sclerosis (ALS). I investigated the intermembrane space (IMS)-UPRmt in G93A-SOD1mousemodel of familialALS, sincemutant SOD1 is known to accumulate in the IMS of neural tissue and cause mitochondrial dysfunction.Using a mouse model in which G93A-SOD1 was selectively targeted to the IMS, I demonstrated that the IMS-UPRmt could be specifically initiated by mutant SOD1 localized in the IMS.
