Dementia is a major cause of disability and dependency among older population. Alzheimer’s disease (AD) is the leading cause of dementia in late adult life. AD’s pathohysiological markers include hyperphosphorylated TAU, accumulation of amyloid-β and elevated oxidative stress markers. Though, many pharmacological treatments are available for AD patients, none inhibit cognitive decline. Hyperbaric oxygen therapy (HBOT) has been shown to alleviate cognitive decline symptoms in AD case studies. Oxygen plays a critical role as a substrate for metabolism and as a signaling molecule regulating cellular activities, but under certain conditions, it is converted to a highly reactive molecule, known as reactive oxygen species (ROS), ready to oxidize other molecules in the cell and cause damage. As HBOT increases the solubility of oxygen in the blood and tissues, it can cause an increase in the levels of ROS. Therefore, it is important to understand what the effects of HBOT on oxidative stress are. Accordingely, we utilized HBOT on a mouse model of AD (5xFAD) to better understand the effects on oxidative stress and antioxidant scavenger enzymes. Our experimental protocol consists of 20 HBO sessions of 1h treatment at 2 Atmosphere absolute over a period of a 1 month that are given for both WT and 5xFAD mice. Following the treatment, we assess oxidative stress, antioxidant enzymes and mitochondrial activity. We found that HBOT treated mice showed a significant elevation in antioxidant (SOD and Catalase) activity in the cortex and we are currently examining other factors. This result supports the hypothesis that HBOT is accompanied by an increase of alleviating mechanisms and increases antioxidant enzymatic activity. Thus, in addition to the mitigating effects of HBOT on AD pathophysiology, it might also be beneficial in reducing the levels of oxidative stress.