The goal of my PURM project was to study the mechanisms of lithium neuroprotection in Alzheimer's Disease. We hypothesized that lithium provides neuroprotection by amelioration of calcium dysregulation in Alzheimer's Disease, associated downstream mitochondria dysfunction, and impairment of neurogenesis. To test this hypothesis I performed cell culture on SH-SY5Y cells, human brain neuroblastoma cells. This cell line is a common model for neurodegnerative disorders because the cells can be easily differentiated into neurons through the addition of specific compounds. I collected the mitochondria oxygen consumption rate from these cells using the Seahorse Mito Stress Test set up. Data from these tests demonstrated that glutamate, a Sporadic Alzheimer's Disease risk factor, significantly impaired mitochondria oxygen consumption rate in the SH-SY5Y cells. Lithium's ability to inhibit this glutamate response and mediated impairment of neurogenesis can serve as a partial mechanism in a therapeutic drug for Alzheimer's Disease.