|Alzheimer's Disease (AD) is a neurodegenerative disease that afflicts the elderly. Three hallmark pathologies of AD include amyloid beta (A-beta) accumulation, inflammation, and oxidative stress. The aggregation of A-beta protein fragments develops plaques in the brain, increasing levels of proinflammatory cytokines. Chronic activation of proinflammatory cytokines increases inflammation, further exacerbating AD pathologies. Oxidative stress is linked to many neurodegenerative diseases, due to an imbalance of the antioxidant system and increased reactive oxygen species (ROS) production, which further damages DNA and chronically activates microglial cells. Past research has shown that antioxidant compounds alleviate proinflammatory cytokine production. The aim of this study was to further explore this by studying the therapeutic capabilities of two potent antioxidant molecules (L2 and L4) in attenuating oxidative stress and inflammation in microglial cells. We hypothesized that L2 and L4 will reduce proinflammatory cytokines induced by LPS treatment.