Alzheimer’s disease (AD) is one of the most common neurodegenerative diseases, affecting over 5 million Americans. This disease is commonly characterized by the formation of senile plaques of the amyloid beta (Aβ) peptide and neurofibrillary tangles commonly developed in the hippocampus, prefrontal cortex, cerebellum, and the temporal lobe, thus endangering the patient’s memory, thinking, language, planning, and behavior. Symptoms generally develop slowly and worsen over time, becoming severe enough to interfere with everyday tasks. There have been multiple hypotheses regarding the development of AD, but there is still no known cause or cure. Treatment has been limited to alleviating the symptoms for those affected by AD. A newer approach focuses on mitochondrial dysfunction, when the mitochondria, the powerhouse of the cell, releases reactive oxidative species (ROS) that cause changes in expression and damage to tissues, proteins, and genes. The principal goal of our research project is to contribute to resolving the mechanism of AD to identify potential targets for a cure. We will evaluate changes in protein expression as a result of exposure to a high oxygen environment, Aβ, and current therapeutics. Changes in protein trafficking and expression are monitored using fluorescence microscopy in conjunction with immunochemistry and Western blot analysis. Our preliminary studies verify that the α7 subtype of nicotinic acetylcholine receptor (nAChR) is upregulated upon exposure to donepezil, a current treatment for AD. Further studies will investigate the effect of donepezil and other treatments on the expression of mitoNEET and other mitochondrial proteins.

Utilizing fluorescence microscopy to evaluate changes in the expression of nicotinic acetylcholine receptors and mitoNEET

Macromolecular Chemistry: The Second Century

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ACS Spring 2020 National Meeting & Expo

The official archive and repository for all ACS Meetings & Expositions abstracts and select posters or presentations.