Bahri Karacay, Ph.D.
Research Associate Professor of Pediatrics – Neurology
Lab: 216A MRC
200 Hawkins Drive
Iowa City, IA 52242
MS, Molecular Genetics, The Ohio State University
PhD, Molecular Genetics, The Ohio State University
Post Doctorate, Hematology & Oncology , Nationwide Children’s Hospital / University of Iowa, Carver College of Medicine
Education/Training Program Affiliations
Interdisciplinary Graduate Program in Human Toxicology
My research focuses on abnormalities in developing nervous systems that are caused by two neuroteratogenic agents: alcohol, (fetal alcohol spectrum disorder -FASD) and lymphocytic choriomeningitis virus (congenital LCMV infection). Fetal exposure to alcohol can severely and permanently damage the developing brain and can lead to fetal alcohol spectrum disorder, a leading cause of mental retardation in the United States. Currently, there are no clinical remedies to prevent the neuronal losses induced by fetal alcohol exposure. Thus, a goal of my research has been to identify agents, genes, and signaling pathways that can prevent alcohol-induced neuronal death in the developing brain. Lymphocytic choriomeningitis virus (LCMV) infection during pregnancy severely injures the human fetal brain. Children with congenital LCMV infection can present with a diverse set of neurological deficits, have a host of neuropathologic abnormalities and a wide range of neurologic outcomes. Our lab developed a rat model for congenital LCMV infection that remarkably recapitulates the human condition. Our goal in this project is to determine the molecular mechanism by which the virus destroys the fetal brain. One of the important finding of LCMV research is that the virus selectively infects astrocytes in the brain, in a region-specific manner, and uses astrocytes as the portal of entry. This finding formed the foundation of the next project: the development of gene therapy for Alexander Disease. Alexander Disease (AlexD) is a disease of cerebral white matter and is caused by an autosomal dominant mutation of the gene for glial fibrillar acidic protein (GFAP), a protein expressed exclusively in astrocytes. Our goal in this project is to silence the mutant GFAP allele using RNAi technology to prevent and/or reverse this debilitating disease.
Stead Family Department of Pediatrics
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