Abstract: Oxidative stress in Alzheimer’s disease: Oxidative stress refers to an imbalance between the pro-oxidative and anti-oxidative states that are part of normal cell metabolism that results in the elevated production of reactive oxygen species (ROS) and free radicals. These products oxidize lipids, proteins, and DNA, significantly threatening the integrity of neurons (Praticò, 2008; Padurariu et al., 2013). Specifically, free radicals such as the superoxide anion (O2•–), hydroxyl radical (OH•), and non-radical molecules including hydrogen peroxide (H2O2) and singlet oxygen (1O2), are often produced in the mitochondria during oxidative phosphorylation and can enter the cytoplasm of the cells and causes damage outside of the mitochondria (Guo et al., 2013; Padurariu et al., 2013). After this step, there is a subsequent reduction in the cell’s endogenous-antioxidant potential along with inhibition of mitochondrial respiration, reduction of  adenosine triphosphate (ATP) levels, mitochondrial bursting, Ca2+ dyshomeostasis, membrane damage, and subsequent production of insoluble aggregate which results in proteotoxicity and protein aggregation (Praticò, 2008; Guo et al., 2013; Padurariu et al., 2013). The brain is particularly vulnerable to the oxidative stress due to its high oxygen requirement and lipid-rich composition. Therefore, damage to the brain caused by oxidative stress has a high chance of impairing normal central nervous system processes and may result in progressive cell damage, neurodegeneration, and cell death (Guo et al., 2013). The term antioxidant often refers to a group of vitamins and synthetic, plant-derived, or inorganic substances that can inhibit the production of, promote the detoxification, or scavenge reactive oxidant species (Praticò, 2008).