Author ORCID Identifier

https://orcid.org/0000-0001-8913-079X

Date Available

11-2-2020

Year of Publication

2020

Degree Name

Master of Science (MS)

Document Type

Master's Thesis

College

Arts and Sciences

Department/School/Program

Psychology

First Advisor

Dr. Mark Prendergast

Abstract

Fetal Alcohol Spectrum Disorders (FASDs) are comprised of developmental, behavioral, and cognitive abnormalities caused by prenatal alcohol exposure, affecting an estimated 2%-5% of childrenand costing up to $4 billion annually in the United States alone. Although some behavioral therapies can help, the biochemical mechanisms that underpin FASDs need further elucidation for development of more efficacious therapeutics. The tau protein modulates cytoskeletal structure in neurons, and thereby plays an integral role in proper development and function of the central nervous system, but its function is altered by its phosphorylation state, such that increased phosphorylation reduces tau protein function. The tau protein is highly phosphorylated at birth but becomes dephosphorylated during structural maturation. Aberrant tau hyperphosphorylation is cardinal of neurodegenerative diseases, but less is known about its role in neurodevelopmental disorders, like FASD. In the neonatal rat model of organotypic hippocampal slice culture, tau phosphorylation decremented in all measured regions of the control hippocampus across 24 days in vitro, but tau hyperphosphorylation was sustained in all regions except the CA3 in hippocampal slices that were exposed to alcohol. Future research should investigate the functional, behavioral, and cognitive relevance of hyperphosphorylated tau protein with regard to FASDs to identify potential therapeutics.

Digital Object Identifier (DOI)

https://doi.org/10.13023/etd.2020.510

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