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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. The cerebellum is a key brain region in relaying motor and sensory signals to the thalamus and the cortex. Guidance cues and guidepost cells aid in the migration of cerebellar 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. Past studies also illustrate that ethanol causes a volume decrease of the cerebellar anterior vermis where guidance cue molecules are concentrated, thus lowering expression. We theorize that axon guidance due to prenatal ethanol exposure alters guidance cue mechanisms in the cerebellum. The Favero lab will produce a review article utilizing the paper sprint model designed by The University of Michigan. The objective of the review article 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, "A Review on Altered Axon Guidance in the Cerebellum due to Prenatal Ethanol Exposure" (2020). Neuroscience Summer Fellows. 17.
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