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10.1111/acer.12051

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C3670687!3670687!23442156
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suck abstract from ncbi


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pmid23442156      Alcohol+Clin+Exp+Res 2013 ; 37 (6): 924-32
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  • The Influence of Fetal Ethanol Exposure on Subsequent Development of the Cerebral Cortex as Revealed by Magnetic Resonance Imaging #MMPMID23442156
  • Leigland LA; Ford MM; Lerch JP; Kroenke CD
  • Alcohol Clin Exp Res 2013[Jun]; 37 (6): 924-32 PMID23442156show ga
  • Background: Fetal alcohol syndrome and related disorders (commonly referred to as Fetal Alcohol Spectrum Disorder, or FASD) cause significant hardships to the individuals affected. Previously, histological studies in animals have characterized developmental cerebral cortical abnormalities that result from prenatal ethanol exposure. Additionally, magnetic resonance imaging (MRI) studies have identified abnormalities associated with fetal ethanol exposure in the cerebral cortices of human children and adolescents. However, there is still a need to bridge the gap between human MRI studies and animal histological studies. The goal of the research presented here was to perform postmortem MRI experiments on rodents, during time periods relative to late human gestation through adulthood, to characterize of anomalies associated with FASD throughout development. Additionally, by determining how histologically-identified abnormalities are manifest in MRI measurements specifically during the critical early time points, neuroimaging-based biomarkers of FASD can potentially be identified at much earlier ages in humans, thus reducing the impact of these disorders. Methods: Cerebral cortical volume, thickness and surface area were characterized by ex vivo MRI in Long-Evans rat pups born from dams that were ethanol-treated, maltose/dextrin-treated or untreated throughout gestation at 6 developmental time points (postnatal day (P)0, P3, P6, P11, P19 and P60). Results: Brain volume, isocortical volume, isocortical thickness and isocortical surface area were all demonstrated to be reduced following prenatal exposure to ethanol. Significant differences among the treatment groups were observed throughout the range of time points studied, allowing for a comprehensive view of FASD influenced MRI outcomes throughout development. Isocortical surface area and isocortical thickness results contributed independent information important to interpreting effects of prenatal ethanol exposure on cerebral cortical development. Additionally, regional patterns in cortical thickness differences suggested primary sensory areas were particularly vulnerable to gestational ethanol exposure. Conclusions: Structural MRI measurements were in accordance with previous histological studies performed in animal models of FASD. In addition to establishing a summary of MRI outcomes throughout development in FASD, this research suggests that MRI techniques are sufficiently sensitive to detect neuroanatomical effects of fetal ethanol exposure on development of the cerebral cortex during the period of time corresponding to late gestation in humans. Importantly, this research provides a link between animal histological data and human MRI data.
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