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dc.contributor.authorNakhleh, Lauren
dc.date.accessioned2019-09-25T20:41:25Z
dc.date.available2019-09-25T20:41:25Z
dc.date.issued2019-05-19
dc.identifier.urihttps://repository.tcu.edu/handle/116099117/26999
dc.description.abstractAlzheimer's Disease (AD) is a progressive neurodegenerative disease that is currently ranked as the sixth leading cause of death in the United States. Those affected by the disease experience symptoms such as cognitive decline, memory loss, confusion, and difficulty with language. Two of the main hallmarks of AD are neuroinflammation and oxidative stress. Inflammation is normally a natural response that aids in fighting off pathogens. However, constant inflammation can be toxic to brain tissue. Oxidative stress is characterized by the accumulation of free radicals and reactive oxygen species (ROS) and can be caused by many mechanisms such as mitochondrial destruction and dysfunction of the antioxidant system. Neuroinflammation and oxidative stress are linked processes that exacerbate one another. For example, the presence of ROS can activate microglia to produce increased levels of pro-inflammatory cytokines. Additionally, both of these processes interact with AD pathology, further contributing to the presence of neurodegeneration. The current study is aimed at investigating whether L2, a powerful antioxidant created in Dr. Kayla Green's lab at TCU, could produce a rebound effect on the viability of microglial cells undergoing oxidative stress and inflammation. BV2 microglial cells were used in conducting the MTT assays performed to measure percent cell survival. First, the oxidative stressor, H202, was administered to the cells at increasing concentrations in order to establish a negative, dose dependent relationship between oxidative stress and cell viability. The second portion of the procedure involved adding L2 compound at increasing concentrations to the microglial cells with a constant concentration of 3.0 µM H202 administered to all wells one hour later. This set-up allows us to measure the potential rescue capacity of L2. Finally, LPS was administered to the cells at increasing concentrations in order to substantiate an inflammatory state in the microglia. H202 was found to be a powerful oxidative stressor, causing substantial cell death. However, LPS did not produce as drastic results, only causing a limited decline in microglial cell viability. Finally, L2 showed a noticeable rescue capacity prior to H202 administration, suggesting a possible future for L2 as a therapeutic method for AD and other neurodegenerative diseases.
dc.titleOxidative Stress as a Target for Alzheimer's Disease Therapeutics
etd.degree.departmentBiology


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