Although Tau is phosphorylated by numerous kinases, evidence indicates that glycogen synthase kinase-3 beta (GSK3β) phosphorylation at Ser199 and Ser202 (pTau-Ser199/202) is a key component of AD pathology and thought to be a viable therapeutic target (Llorens-Martin, Jurado, Hernandez, & Avila, 2014). Interestingly, GSK3β is an alcohol-sensitive gene (Wolen et al., 2012) and phosphoprotein (Cheng et al., 2017; Liu et al., 2017) in a variety of brain regions, including the HPC of adult mice exposed to prenatal alcohol (Cunningham et al., 2017). Therefore, we asked if Tau phosphorylation at the GSK3β (Ser199/202) site is altered by alcohol drinking in 3xTg-AD mice, which would indicate a potential target of alcohol.
