Hi, I’m Ada! Welcome to my research page!
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I am a member of the Princeton High School 3 year research program! I have always had a strong passion for understanding the molecular mechanisms that explain why medical phenomena occur. Specifically, the role of trace metal imbalances in the pathogenesis of Alzheimer’s Disease has peaked my interest. After spending year one reading dozens of publications in this field, I developed a research procedure to test my own hypothesis that amyloid-beta aggregations increase as a protective homeostatic mechanism when trace metals copper and zinc increase beyond their homeostatic range in Alzheimer’s Disease. I networked with professors at surrounding universities when any procedural challenges occurred. The materials I needed required over $2,250 of funding. Therefore, during year 2, I fundraised through the crowdfunding website experiment.com. I spent six months fundraising, contacting manufacturers about material specifications, and ordering materials. The second half of year 2 involved conducting experimentation. The third year has been comprised of communicating my findings!
Experiment.com profile: https://experiment.com/tracemetalsalzheimers
Alzheimer’s Disease (AD), a progressive neurodegenerative disease characterized by the buildup of amyloid-beta (Aβ) plaques, is believed to be a disease of trace metal dyshomeostasis. Amyloid-beta is known to bind with high affinity to trace metals copper and zinc. This binding is believed to cause a conformational change in Aβ, transforming Aβ into a configuration more amenable to forming aggregations. Currently, the impact of Aβ-trace metal binding on trace metal homeostasis and the role of trace metals copper and zinc as deleterious or beneficial in AD remain elusive. Given that Alzheimer’s Disease is the sixth leading cause of adult death in the U.S., elucidating the molecular interactions that characterize Alzheimer’s Disease pathogenesis will allow for better treatment options. To that end, the model organism C. elegans is used in this study. C. elegans, a transparent nematode whose connectome has been fully established, is an amenable model to study AD phenomena using a multi-layered, interconnected approach. Aβ-producing and non-Aβ-producing C. elegans were individually supplemented with copper and zinc. On day 6 and day 9 after synchronization, the percent of worms paralyzed, concentration of copper, and concentration of zinc were measured in both groups of worms. My research demonstrates that dyshomeostasis of trace metals copper or zinc triggers further trace metal dyshomeostasis in Aβ-producing worms, while dyshomeostasis of copper or zinc triggers a return to homeostasis in non-Aβ-producing worms. This supports the characterization of Alzheimer’s Disease as a disease of trace metal dyshomeostasis.