Alzheimer’s Disease (AD) is a neurodegenerative disease caused by a number of factors. One of the leading factors behind the onset of AD is the accumulation of amyloid plaques in the brains of affected individuals. These plaques are formed with amyloid precursor protein (APP) is processed incorrectly and cleaved to be 42 amino acids long (Aβ42) instead of 40 (Aβ40). These two extra amino acids cause the protein to become hydrophobic in nature and form plaques which aggregate around neurons in the brain. This aggregation induces oxidative stress on the neurons which then leads to cell death. Due to the conserved genetic properties of the Drosophila melanogaster, fruit fly, visual system with that of humans we have developed a Drosophila eye model. In this model the Aβ42 protein is misexpressed in the developing photoreceptors of the fly eye which results in extensive cell death of the photoreceptor neurons and produces a highly reduced eye field in the adult fly. Our aim is to understand the function of a soy protein called Lunasin in Alzheimer’s disease. It has been shown that Lunasin acts as an anti-inflammatory within the somatic cells. Inflammation is also one of the characteristic of AD. Therefore, we investigated the effects of Lunasin on Aβ42 accumulation mediated neurodegeneration. We found that Lunasin can rescue the Aβ42 mediated neurodegeneration in the retinal neurons as well as the axonal targeting from the retina to the brain. We are looking into the mechanism of this Lunasin mediated rescue.