Susan M. Smith, PhD

About

Dr. Smith studies how nutrition impacts the fetus, and how nutrition, genetics, and prenatal alcohol exposure (PAE) interact to impair fetal development. PAE affects 3.9% of U.S. births and causes perisistent behavioral and cognitive impairment. At the molecular level, her lab identified the molecular signals through which alcohol causes the apoptotic deletion of craniofacial stem cell precursors (aka “the neural crest”), a diagnostic feature of PAE. Current work studies the MDM2/p53/ribosomal gene network that modulates neural crest vulnerability to alcohol’s damage. Her lab has also isolated maternal iron-deficiency (ID) as a risk factor that heightens fetal vulnerability to PAE-induced learning deficits. Other projects explore how PAE affects risk for metabolic syndrome and eating disorders in adolescence and adulthood. Her work is recognized by a prestigious MERIT award from NIAAA. She serves on the External Advisory Council for NIAAA, and is past chair of the NIH Neurotoxicology and Alcohol (NAL) study section and past-president of the Fetal Alcohol Spectrum Disorders Study Group.

Susan Smith in the Gillings News

Key Publications

Prenatal alcohol exposure alters fetal iron distribution and elevates hepatic hepcidin in a rat model of fetal alcohol spectrum disorders. Huebner SM, Blohowiak SE, Kling PJ, Smith SM (2016). J. Nutrition, 146.
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Significantly dysregulated eating behavior and hyperphagia in children with prenatal alcohol exposure. Amos-Kroohs R, Fink B, Smith CJ, Van Calcar SC, Wozniak JR, Smith SM (2016). J. Pediatrics, 169.
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An evolutionarily conserved mechanism of calcium-dependent neurotoxicity in a zebrafish model of fetal alcohol spectrum disorders. Flentke GR, Klingler RH, Tanguay RL, Carvan MJ 3rd, Smith SM (2014). Alcoholism: Clinical and Experimental Research, 38(5), 1255-65.
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High-throughput transcriptome sequencing identifies candidate genetic modifiers of vulnerability to fetal alcohol spectrum disorders. Garic A, Berres ME, Smith SM (2014). Alcoholism: Clinical and Experimental Research, 38(7), 1874-82.
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Genomic factors that shape craniofacial outcome and neural crest vulnerability in FASD. Smith SM, Garic A, Berres ME, Flentke GR (2014). Frontiers in Genetics, 7(5), 224.
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CaMKII represses transcriptionally active β-catenin to mediate acute ethanol neurodegeneration and can phosphorylate β-catenin. Flentke GR, Garic A, Hernandez M, Smith SM Journal of Neurochemistry, 128(4), 523-35.
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Adequacy of maternal iron status protects against behavioral, neuroanatomical, and growth deficits in fetal alcohol spectrum disorders. Rufer ES, Tran TD, Attridge MM, Andrzejewski ME, Flentke GR, Smith SM (2012). PLoS One, 7(10), e47499.
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Education