Alzheimer’s disease (AD) is a chronic neurodegenerative condition that affects nearly 44 million people worldwide. The hallmark of Alzheimer’s pathology is the accumulation of extracellular Amyloid Beta 42 (Aβ42) protein plaques generated by defective endoproteolysis of amyloid precursor protein (APP) by α– and γ-secretase. We misexpressed human Aβ42 in the third instar larval eye imaginal disc of Drosophila. This stable transgenic line results in GMR-GAL4 driven Aβ42-mediated cell death in the eyes of nearly 100% of adult flies. In a forward genetic screen, we identified the Ecdysone signaling pathway as a modifier of neurodegeneration caused by Aβ42 accumulation in the eye. It has been shown that Ecdysone (Ecd) signaling pathway modulates Hippo transcriptional activity in imaginal disc cells. Our preliminary data suggests that upregulation of the involved Yki-Tai transcription complex rescues Aβ42-mediated neurodegeneration in our Drosophila eye model. We propose to understand the underlying molecular genetic mechanism responsible for Ecd/Hippo-mediated rescue of Aβ42 mediated neurodegeneration.