Alzheimer's disease (AD) is a common form of brain disease leading to loss of cognitive functions with symptoms including loss of memory, behavior changes, and confusion. Previous studies have suggested a link towards metabolic alterations and mitochondrial dysfunction and Alzheimer's (AD). Therefore, we hypothesize that stabilizing these signaling pathway can give us insight into possible treatment for Alzheimer's Disease. The parameters for this evaluation included a single dose of the Streptozotocin (STZ) (3mg/kg) intracerebral ventricular injection within mice for induction of AD. For the treatment groups, STZ-AD mice were also treated with vehicles or PKC inhibitor LY333531 (orally, 1 mg/kg/day) or mitochondria ROS (mROS) inhibitor Mito-Tempo (IP injection, 1 mg/kg/day). In the last 5 days of a 28 day period, the induced STZ-AD and treatment groups were all given the Morris water maze test followed by brain harvest for protein analysis. Within STZ-AD mice, they exhibited higher escape latency and lower path efficiency than the control mice, allowing us to recognize damaged cognitive function. Interestingly, within both treatments of the PKC and mROS inhibitors, the escape latency was partially restored, suggesting an improvement in cognitive function. For protein analysis, we expect to see a decrease in Tau proteins within the treated groups, as well as a decrease within apoptosis signaling. Our work has demonstrated that with the use of PKCαβ or mROS inhibitors, STZ- induced AD mice had the escape latency partially restored. Further analysis within these treatment groups can provide substantial information on possible treatment for Alzheimer's disease.