The Ori-McKenney lab will study the mechanisms that trigger dementia and neurodegeneration following traumatic brain injury. Even a single blow to the head can cause traumatic brain injury, which is in part characterized, on a molecular level, by the addition of an excess of phosphate groups to a protein called tau. Although it has been observed that following brain injury, tau becomes phosphorylated at positions recognized by a protein called GSK-3 beta, our lab has discovered, in a preliminary study, that another protein, called DYRK1a, may get there first—and enhance subsequent phosphorylation by GSK-3 beta, while inhibiting phosphorylation by another kinase. Using sophisticated methods in biochemistry, neuroscience, and molecular genetics, we will dissect the signaling events that lead to the elevated phosphorylation of tau in vinegar flies subjected to traumatic brain injury. Our group will explore how this modification affects tau activity, how phosphorylation of tau at different sites alters the locomotion and life span of the flies, and whether drugs that target DYRK1a offer protection from neural damage. Because DYRK1a also contributes to neurological diseases such as Alzheimer’s, our findings could hasten the development of treatments for a variety of neurodegenerative conditions.