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Alzheimer’s disease (AD) is a neurodegenerative disease that affects more than five million individuals in the United States alone, where it is the sixth leading cause of death. While there is currently no cure for the disease, it is a highly investigated topic of research. The Drosophila melanogaster eye model is an excellent system to study AD, due to the highly conserved genetic machinery shared between flies and humans. We have developed a transgenic fly model of AD in which we use the GAL4/UAS system to misexpress high levels of human Aβ42 peptides in the differentiating photoreceptor neurons in the fly eye. We use this system to determine whether modulating the function of the calcium signaling pathway can modify Aβ42 mediated neurodegeneration. We used RNAi to knock down six components of the calcium signaling pathway (stim-RNAi, serca-RNAi, orai-RNAi, inx2-RNAi, ip3r-RNAi, and plc 21c-RNAi) in an Aβ42 background in the eye and observed the effects in both eye antennal imaginal discs and adult eyes. Our results showed evidence that knocking down components of the calcium signaling pathway may ameliorate the neurodegeneration mediated by Aβ42. Aberrant calcium signaling has also been implicated in cancer and other neurological diseases besides AD. Our research further implicates intracellular calcium signaling in neurodegenerative disorders such as AD. Further research will determine the molecular mechanisms linking calcium signaling with Aβ42 mediated neurodegeneration.
Primary Advisor's Department
Stander Symposium poster
"Role of calcium signaling in Aβ42-mediated neurodegeneration in a Drosophila model of Alzheimer’s disease" (2019). Stander Symposium Posters. 1522.