Beyer, RachelAldhubayb, Meshal2018-12-202018-12-202018-12-19http://hdl.handle.net/11603/12327In this study, we investigate the role of LIMP-2 in decreasing the cytotoxicity of the alpha-synuclein in the familial mutations of the alpha-synuclein in Parkinson’s disease models.Parkinson’s disease is a slow aggressive neurological disorder characterized by loss of dopamine in substantia nigra which is located in the brain and formats a neuronal cytotoxic protein called alpha- synuclein. Researchers found that genetics plays a significant role in formation of alpha-synuclein aggregation. Studies of families with the history of Parkinson’s disease have identificatied of familial mutations (A30P, E46K, H50Q, G51D, A53T). Researchers have tried to prevent alpha-synuclein aggregation as a way to treat Parkinson’s disease. One possible and promising way to prevent aggregation is overexpression of the lysosomal Integral Membrane Protein type-2 (LIMP-2). In this project, I propose to investigate the role of LIMP-2 in the familial mutation of Parkinson’s diseases. This project uses cellular models for each of the familial mutations for Parkinson’s diseases, inserts of plasmids that contain the LIMP-2 to these cellular models to investigate the effect of the LIMP-2 added on proved aggregation in the familial mutations, and monitor alpha-synuclein aggregation by using Fluorescence Resonance Energy Transfer (FRET) to measure it.en-USAttribution-NonCommercial 3.0 United StatesALPHA-SYNUCLEIN AGGREGATIONCollection