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dc.contributor.authorKinsinger, Olivia
dc.date.accessioned2020-08-24T15:57:01Z
dc.date.available2020-08-24T15:57:01Z
dc.date.issued2020-05-19
dc.identifier.urihttps://repository.tcu.edu/handle/116099117/40326
dc.description.abstractIt is estimated that 45% of people over the age of 85 in the U.S. suffer from Alzheimer?s disease. Patients with Alzheimer?s disease, which is characterized by cognitive deficiencies and memory loss, have higher concentrations of amyloid plaques in brain tissue than patients without the disease. Abnormal levels of transition metal ions Fe, Zn, and Cu in brain tissue are associated with amyloid beta plaques and also have been shown to catalyze the generation of excess reactive oxygen species (ROS) and cause oxidative stress. The combination of the ROS generation and the amyloid plaque formation results in neuronal cell death and subsequent neurodegeneration, which ultimately causes the memory loss and death associated with Alzheimer?s. We have synthesized the compounds L2 and L4 which are designed to chelate metal ions and scavenge ROS, thus reducing the damage they cause. We hypothesize that due to their chelating properties and pyridol groups, L2 and L4 should reduce oxidative damage in neuronal cells by chelating metal ions and scavenging free radicals.  The cytotoxicity of the compounds was first tested on HT-22 neuronal cells. Next, neuronal cells were treated with,compounds that induce formation of ROS, in the presence and absence of L2 and L4. If our hypothesis is correct, our compounds should reduce the oxidative damage induced by these compounds.
dc.titleReducing ROS and Chelating Metal Ions in Neuronal Cells Using Novel Compounds


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