University of Tasmania, Australia

Honours

Additional Information

The Intersection of Oxidative Stress and Autophagy in Neurodegenerative diseases

Neurodegenerative diseases such as Parkinson's Disease and Huntington's Disease are well established to be linked with protein aggregate formation and oxidative stress. Aggregated proteins are usually removed from the cell by macroautophagy, where by p62 binds to ubiquitinated proteins and LC3-II which is then engulfed by an autophagosome. A lysosome then fuses with the autophagosome and leads to protein degradation. Oxidative stress of the other hand is mediated by NRF2-KEAP1 where in oxidative conditions, KEAP1 dissociates from NRF2 and allows NRF2 to be a trascription factor and increase the expression of antioxidant genes to alleviate the cell from oxidation. One of the proteins produced in this antioxidant response is p62 that competitively binds to KEAP1, and the activation of NRF2 inhibits autophagy. In this study, we aim to compare NRF2 response among drugs, induce autophagy in transfected cells and, finally, investigate drug specific autophagy inhibition in transfected cells.