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dc.contributor.supervisorDel Bigio, Marc R. (Pathology)en_US
dc.contributor.authorBasalah, Duaa Ali
dc.date.accessioned2015-04-06T20:47:29Z
dc.date.available2015-04-06T20:47:29Z
dc.date.issued2015-04-06
dc.identifier.urihttp://hdl.handle.net/1993/30346
dc.description.abstractBackground: Prenatal ethanol exposure (PNEE) causes irreversible intellectual and behavioral disabilities, clinically known as fetal alcohol spectrum disorder. Few neuropathologic studies of human brain exist. Hypotheses: First, markers of oxidative stress persist following PNEE. Second, PNEE is associated with inhibitory and excitatory neuron changes. Methods: Human brain autopsies (153) with known PNEE were reviewed; 18 cases (fetus to adult) and controls were selected. Oxidative stress and neuronal differentiation markers were used for immunohistochemistry. Results: There were no obvious differences between control and PNEE brains using oxidative stress markers. In human PNEE brains, glutamatergic neurons were reduced 15.96 % and 18.03% in dentate gyrus and temporal cortex, respectively. GABAergic neurons reactive for parvalbumin were reduced in all hippocampal regions (CA1= 57.86%, CA3= 65.15%, and DG= 53.39%) and temporal cortex (44.13%) in all age groups. Conclusion: GABAergic neuron reduction in human following PNEE could explain motor and behavior distractibility in FASD individuals.en_US
dc.language.isoengen_US
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectPrenatal Ethanol Exposureen_US
dc.subjectFetal Alcohol Spectrum Disordersen_US
dc.titleOxidative stress and neuronal changes associated with prenatal ethanol exposure in human and monkey brainsen_US
dc.typeinfo:eu-repo/semantics/masterThesis
dc.typemaster thesisen_US
dc.degree.disciplinePathologyen_US
dc.contributor.examiningcommitteeKrawitz, Sherry (Pathology) Rastegar, Mojgan (Biochemistry & Medical Genetics)en_US
dc.degree.levelMaster of Science (M.Sc.)en_US
dc.description.noteMay 2015en_US


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