Alzheimers disease (AD) is the only cause of death among the top 10 diseases that cannot be prevented, cured, or slowed with the current treatments available. Amyloid beta is thought to be the main initiator of AD cognitive decline, activating internal pathways which lead to inflammation, oxidation, and cell death. The objective of this study was to determine if pretreatment of human SH-SY5Y neuroblastoma cells, a model for AD, with antioxidants thymoquinone (TQ), epigallocatechin-3-gallate (EGCG), or dilinoleoylphosphatidylcholine (DLPC) 30 minutes prior to a challenge with tumor necrosis factor a (TNFa), an inflammatory mediator, can prevent oxidation of amyloid beta (Aß). Following treatment, cells were incubated and groups evaluated at 24, 48, and 72 hours. Human amyloid precursor protein (APP) enzyme-linked immune-sorbent assay (ELISA) and nitric oxide assays were performed from supernatant whereas protein and glutathione assays were performed from cells. When TNFa was added to cells, Aß significantly increased 3-fold compared to untreated cells. The addition of antioxidants EGCG, TQ, and DLPC reduced Aß back toward control value at the initial time point. TNFa also caused a significant increase in nitric oxide without changes in glutathione. TQ administered to the cells prior to a challenge with TNFa resulted in a decrease in nitric oxide and an increase in glutathione which may be a possible mechanism to reduce inflammation and reduce oxidation. Additional studies are needed to determine the signaling pathways implemented in the SH-SY5Y cells following TNFa.