Psychology and Neuroscience major Abigail Wilcox has worked in the laboratory of Dr. Mark Prendergast, Professor of Psychology and Director of the Neuroscience B.S. Program, since the 1st year of her studies at UK. Working closely with graduate student Caleb Bailey, Abby and Caleb received a pilot grant from the UK Substance Use Priority Research Area (SUPRA) to investigate a new possible biochemical mechanism involved in the development of Fetal Alcohol Spectrum Disorders.
This worked confirmed that exposure of newborn brain to high doses of alcohol causes abnormalities in brain "tau" activity, much like that seen in Alzheimer's Disease. Congratulations to Abby ! Abby graduated in May of 2022 and is off to a career in applying her Psychology training in the Marketing field.
The University of Kentucky Department of Psychology is home to Internationally-renowned scientists who work with undergraduate student researchers daily to advance our understanding of the brain and its impact on behavior ! Come join us
For more details on the publication, see below
Ethanol sustains phosphorylated tau protein in the cultured neonatal rat hippocampus: Implications for fetal alcohol spectrum disorders
Fetal Alcohol Spectrum Disorders (FASDs) are comprised of developmental, behavioral, and cognitive abnormalities caused by prenatal alcohol exposure, affecting an estimated 2%-5% of children and costing $4 billion annually in the United States. While some behavioral therapies help, the neurobiological mechanisms that underpin FASDs need further elucidation for development of efficacious pharmacotherapeutics. The role of the tau protein in the hippocampus is likely to be involved. Tau catalyzes microtubule polymerization in developing neurons. However, this function can become disrupted by hyperphosphorylation. Many of the cognitive deficits observed in neurodegenerative tauopathies overlap to some degree with what is observed in juvenile developmental disabilities, such as FASDs (e.g., selective memory, executive dysfunction). Thus, tau protein phosphorylation may be one important mechanism of dysfunction in FASDs. The purpose of this study is to provide an empirical basis for a tauopathic characterization of FASDs. To do so, hippocampal slices were extracted from rats at postnatal day 10 (PND10); hippocampal slices were then exposed to 5 days of 50mM ethanol between 6 days in vitro (DIV) and 11DIV. Immunoblots were taken for Total and p-Tau (Threonine231) at 12DIV and 24DIV. Immunohistochemical fluorescent images were taken for p-Tau (Threonine231) at 12DIV and 24DIV. Separate p-Tau measures were taken for the cornu ammonis 1 (CA1), CA3, and dentate gyrus (DG). Total Tau protein expression remained unchanged between 12DIV and 24DIV regardless of EtOH condition. In the control group, longer DIV was associated with decreased p-Tau. However, in the EtOH-exposed group, p-Tau was sustained across DIV. This is the first study to show that EtOH exposure sustains tau Threonine231 phosphorylation in the perinatal hippocampus regardless of total tau expression. These findings could lead to innovative pharmacotherapeutic targets for the treatment of cognitive deficits seen in FASDs.