Presenter(s)

Neha Gogia, Chris Y Kang, Dena M Schaeffer

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Description

Alzheimer’s Disease (AD) is a neurodegenerative disease, common in more than five million individuals in the United States (US) alone, making it the sixth leading cause of death in the US. While currently there are no cures for the disease, there are many ongoing studies, which are using the Drosophila melanogaster model, to find a way to prevent and slow down AD. We have used Drosophila as our model organism; Drosophila eye as our model organ (due to highly conserved genetic machinery between flies and humans). We have developed a transgenic fly model of AD where we misexpress high levels of human Aβ42 peptides using GAL4/UAS system approach, using this system, misexpression is targeted in the differentiating photoreceptor neurons in the Drosophila eye and can be explained to address questions pertaining to whether activating or deactivating certain pathways can rescue Aβ42 mediated neurodegeneration. We have found that members of calcium signaling pathway acts as the modifier of Aβ42 mediated neurodegeneration. In order to test our hypothesis, we misexpressed the loss-of-function form (using RNAi) of six components of calcium signaling pathway (which are stimRNAi, sercaRNAi, oraiRNAi, inx2RNAi, ip3rRNAi, and plc 21cRNAi) in Aβ42 background in the eye, and observed the effects in both eye-antennal imaginal discs and adult eyes. Our results showed 100% eye rescue with all 6 components of calcium signaling pathway at 29C, which clearly states that inactivation of calcium signaling pathway blocks Aβ42 mediated neurodegeneration. Previous studies on calcium signaling pathway showed a role in deadly diseases like cancer and other fatal diseases. Our studies show a new role of calcium signaling in neurodegeneration disorder like AD.

Publication Date

4-18-2018

Project Designation

Independent Research

Primary Advisor

Amit Singh

Primary Advisor's Department

Biology

Keywords

Stander Symposium project

Role of Calcium Signaling Pathway in Rescuing Aβ42 Neurodegeneration in Drosophila

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