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Epigenetics and Fetal Alcohol Syndrome
| CO-PI(s): | M. Michele Pisano |
University of Louisville
Each year in this country nearly a quarter of a million babies are born with some mental or physical anomaly. Despite ongoing research, the causes of nearly seventy percent of birth defects are unknown! What is known is that a woman' s health plays a major role in the outcome of her pregnancy and on the infant's growth and development both pre-and postnatally. Consumption of alcohol during pregnancy leads to fetal alcohol syndrome (FAS), a constellation of congenital anomalies characterized by craniofacial dysmorphology, growth retardation, brain damage and other physical abnormalities. Although FAS is a major nongenetic cause of birth defects, the cellular, biochemical, and molecular mechanisms of alcohol-induced developmental toxicity, and the genes that influence developmental sensitivity to alcohol exposure have not been clearly identified. Recent experimental findings imply that, apart from genetic and environmental factors, epigenetic mechanisms such as DNA methylation might also be associated with the etiology of a range of diseases and developmental abnormalities including FAS. Thus, alcohol-associated modifications in fetal DNA methylation may contribute to the developmental abnormalities seen in the fetal alcohol syndrome. The global hypothesis we plan to address in the current research project is that prenatal (in utero) alcohol exposure can disrupt the normal methylation state of specific candidate genes, in embryonic cranial/forebrain neural folds and contribute to development of fetal alcohol syndrome.
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