Alzheimer’s disease (AD) is a neurodegenerative disease that affects over 5 million Americans. The disease is characterized by the formation of senile plaques of the amyloid beta and neurofibrillary tangles within the brain that can impair the patient’s memory and behavior. These symptoms of AD develop slowly and worsen over time. Currently there is no known cause or cure for AD, therefore treatment is restricted to alleviating symptoms. A new approach to treating AD focuses on mitochondrial dysfunction, occurring when the mitochondria release reactive oxidative species that cause damage and changes to the expression of tissues, proteins, and genes. MitoNEET is a newly discovered mitochondrial protein that is thought to regulate bioenergetics in cells. The focus of our research is to identify if mitoNEET can serve as a potential target for treatment of AD. Fluorescence microscopy was used to assess changes in mitoNEET expression when exposed to current AD therapeutics, including donepezil, rivastigamine, and galantamine. Mouse neuroblastoma cells, N2a cells, were transiently transfected for 24 hours with a mitoNEET-GFP plasmid at a concentration of 150 ng/µL in the trials with donepezil. Then the trials for the rivastigamine and galantamine the N2a cells were transiently transfected for 24 hours with 100 ng/µL of mitoNEET-GFP. Once the transfection mix was removed, the N2a cells were exposed to their designated treatment for 24 hours and imaged. The results showed no change in mitoNEET expression when exposed to 5, 50, 500 µM of donepezil and rivastigamine, and 0.1, 1, 10, 100 µM of galantamine compared to a control with no treatment exposure. Further studies will investigate mitoNEET regulation in response other AD therapeutics.

Analysis of the effect of Alzheimer’s disease therapeutics on mitoNEET expression

ACS Spring 2022

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