The Laboratory conducts a range of studies related to the metabolism and effects of docohexaenoic acid (DHA), an omega-3 polyunsaturated fatty acid. DHA promotes the accumulation of phosphatidylserine (PS), which prevents neuronal cell death. Conversely, dietary deficiencies and long term ethanol exposure both deplete PS from neuronal membranes and accelerate apoptosis. The Laboratory is interested in the structure and function of Akt, a protein that mediates DHA’s antiapoptotic effects. The Laboratory has found that Akt undergoes significant conformational changes at each step in the activation process, and it has identified the protein’s phosphorylation domains. In particular, the serine residue at position 473 (S473) is an important phosphorylation site for Akt activation. The Laboratory has conducted high-throughput screening of molecular libraries to identify compounds that interact with S473, in the hope of developing therapies that promote neuronal longevity.  Additionally, the laboratory has examined docosahexaenoylethanolamide (DEA), a metabolite of DHA, and it has found that DEA promotes neurite development, synaptogenesis and glutamate receptor expression in murine hippocampal neurons. Conversely, feeding mice DHA-deficient diets inhibits neurite development in the hippocampus. The Laboratory’s work also suggests that DHA plays an important role in expression of a number of plasma membrane proteins, and that DHA-related upregulation of PS is specific to neuronal cells. Finally,the Laboratory has found that ethanol exposure decreased the salsolinol levels in the striatum and nucleus accumbens of alcohol-preferring rats. This is an unexpected result, because salsolinol is considered a potential biomarker for alcoholism.