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Fetal Alcohol Spectrum Disorder (FASD) is characterized by physical and neurological deficits as a result of prenatal alcohol exposure. Exposure to alcohol during fetal development can result in sensory and motor processing anomalies. Guidance cues and guidepost cells aid in the migration of axons to their respective locations in the brain for successful signal transduction. Specifically, protein/receptor guidance cue molecules that we will be analyzing are Semaphorin 3A/Neuropilin-1, Netrin/DCC, and Slit/Robo. Past studies observe altered axon guidance when ethanol inhibits axonal growth cones response to guidance cues such as Semaphorin 3A. We theorize that axon guidance due to prenatal ethanol exposure alters guidance cue mechanisms in key brain regions. The Favero lab will produce a review article utilizing the paper sprint model designed by The University of Michigan. This presentation includes information on altered axon guidance in the hippocampus, the cortex, and the cerebellum. The objective is to determine whether FASD alters mechanisms and pathways associated to axon guidance in various key regions of the brain that cause cognitive and behavioral deficits. It is imperative to study the mechanisms of axon guidance as a possible reason for cognitive and behavioral deficits in individuals with FASD.
Mathews, Erin; Dewees, Kevyn; and Diaz, Deborah, "Altered Axon Guidance in Fetal Alcohol Spectrum Disorder: A Review" (2020). Neuroscience Presentations. 7.
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