Research in the Sulik laboratory is directed toward achieving a better understanding of the mechanisms, pathogenesis, and pathology associated with birth defects involving the brain and face. The teratogenic insult resulting from acute maternal ethanol exposure at early stages of embryogenesis is of particular interest. This work employs a mouse model in which salient dysmorphological features of Fetal Alcohol Spectrum Disorder are induced. State of the art imaging methodologies that allow both qualitative and quantitative analyses are utilized (see figures below). More specifically, in collaboration with Duke University's Center for In Vivo Microscopy (http://www.civm.duhs.duke.edu/), high resolution magnetic resonance imaging (MRI) and Diffusion Tensor Imaging (DTI) are employed to identify, characterize, and correlate the craniofacial and CNS dysmorphology in fetal and postnatal mice. Functional and behavioral correlates are also being explored. Overall, these studies are designed to inform human clinical research and to expand diagnostic criteria for Fetal Alcohol Syndrome and Fetal Alcohol Spectrum Disorder. This work is supported by NIAAA and is conducted as part of its Collaborative Initiative on Fetal Alcohol Spectrum Disorder (http://www.cifasd.org/).
Figure 1. High-resolution magnetic resonance imaging (MRI) of fetal mice illustrates exposure-stage-dependent brain and facial dysmorphology resulting from acute ethanol insult on gestational day (GD) 7 versus 8.5 and show that there is not a single pattern of alcohol-induced facial dysmorphology (Lipinski, et al, submitted).
Figure 2. Dense surface modeling studies conducted in collaboration with Dr. Peter Hammond, University College London, illustrate alcohol exposure-stage-dependent correlative changes in the face and brain (esp. the septal region and olfactory bulbs) (Lipinski, et al, submitted).
Figure 3. High resolution MRI of fetal mice readily illustrates the broadly ranging degree of insult that can result from alcohol exposure at specific stages of embryogenesis. (O'Leary-Moore, et al, 2011).
Figure 4. The corpus callosum dysmorphology resulting from GD 7 exposure is strikingly similar to that published for children with FAS (O'Leary-Moore, et al 2011). Thus it is clear that the defects caused by early prenatal alcohol exposure in mice are both persistent and pertinent to humans.
In addition to basic research, efforts directed toward FASD prevention have entailed development of science-based curricula. The first, entitled “Better Safe Than Sorry: Preventing a Tragedy” was created for middle school-age audiences and is freely available on the NIAAA website at http://pubs.niaaa.nih.gov/publications/Science/curriculum.html. The second, entitled "An Ounce of Prevention" was created for high school-age science, health, and parenting classes and will be available in the near future.
Bowles Center for Alcohol Studies at the University of North Carolina at Chapel Hill