The goal of my research is to determine whether 3BDO, a well established drug in the field of Alzheimer's research, can reverse the detrimental effects of Beta-Amyloid overexpression. Beta-Amyloid is a naturally occurring protein whose role is not fully understood, but its overexpression is key to neuronal deterioration, a major symptom of Alzheimer's Disease.
Alzheimer’s disease affects the health and function of neurons in the brain and leads to a decline in a person's ability to recall and consolidate information. Neurons relay information to each other through their synapses. Over time, neural pathways or patterns of firing are created as the result of repetitive movement or thought processes. If the cell is damaged, its functions are hindered, and it cannot perform its duty to organize and process information. In Alzheimer’s, Beta-Amyloid is a protein that becomes overexpressed extracellularly, and leads to damage in cell function. 3BDO is a compound that has been shown to activate the nucleolus, a part of a cell that is responsible for producing PARP-1, a protein that helps with the consolidation of long-term memory. Previous work has shown that 3BDO can prevent damage to the nucleolus. The goal of this project is to look at how effective 3BDO can be for reversing damage to cells. HEK cells, an immortalized line of cells derived from the kidney, will be starved to mimic the damage expressed by Beta-Amyloid in Alzheimer’s. Then, the cells will be incubated in 30µM, 60µM, and 120µM of 3BDO solution for 24 hours to observe the effects of 3BDO post-impairment. HEK cells are used because they are easy to reproduce and maintain in high numbers. We expect to see positive effects with 3BDO similar to the effects seen with prevention of Beta-Amyloid induced damage by 3BDO.
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