Two clone system to study cell-cell communication between wild-type and amyloi-beta 42 plaque forming cells in Alzheimer's disease.

Title

Two clone system to study cell-cell communication between wild-type and amyloi-beta 42 plaque forming cells in Alzheimer's disease.

Authors

Presenter(s)

Jordan C Dubbs, Sean A Kelly, Nilan Mani, Ankita Sarkar

Files

Description

Alzheimer’s is a neurodegenerative disease caused by the miscleavage of the Amyloid precursor protein (APP). When the APP protein is properly cleaved it forms Aβ40 protein, and when it is improperly cleaved it forms the Aβ42 protein that is 2 extra amino acids long. This causes the formation of plaques within the neuron cells and leads to cell death and ultimately large scale changes in the brain tissue. We have designed a genetic system where we have combined strength of FLP/FRT system with the Gal4/UAS –system to target Aβ42 cells in the developing retinal neurons of the developing eye. Misexpression of Aβ42 results in strong neurodegenerative phenotype. Using our newly developed system we are making two types of clones by FLP FRT mediated recombination where one clone of cells is marked by strong presence of GFP reporter and express high levels of Aβ42 whereas the other clone of cells which are marked by the absence GFP are wild-type retinal neurons. The purpose of the Two Clone System is to track the progression of Alzheimer and Wild Type cells within the eye imaginal disc of D. melanogaster. The system was developed to see if the rate of progression of Wild Type cells and Alzheimer's cells would be equal. Furthermore, using markers for various signaling pathways we will test if there is a signal emanating from Aβ42 expressing cells that trigger neurodegeneration. The results from these studies will be presented.

Publication Date

4-5-2017

Project Designation

Independent Research - Graduate

Primary Advisor

Amit Singh

Primary Advisor's Department

Biology

Keywords

Stander Symposium poster

Two clone system to study cell-cell communication between wild-type and amyloi-beta 42 plaque forming cells in Alzheimer's disease.

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