My lab focuses its research efforts on the cellular mechanisms that trigger and contribute to neuronal death and dysfunction. We use a combination of in vivo (transgenic and toxin mouse models) and in vitro (primary brain cultures, including neurons, glia, and neural progenitor/stem cells) experimental approaches to investigate the over-arching idea that dysregulation of kinase pathways and subsequent transcriptional activation/inhibition contribute to neuronal death and dysfunction, and that small molecule approaches to modulating these signaling pathways are viable therapeutic approaches to enhancing neuronal function and survival in a number of neurological/psychiatric disease states. Calcium deregulation, oxidative stress and mitochondrial dysfunction are among the causes often implicated in neuronal death, and are also under study in the lab. Overall, we seek to understand both the molecular events contributing to neurodegeneration as well as the mechanisms by which neurons protect themselves from such damage. Our goal is to develop therapeutic strategies, based on modulation of these signaling pathways, for the prevention/treatment of neurodegenerative and neuropsychiatric diseases.