Nutritional Impact on Rotenone-induced Parkinson's Disease in a Drosophila melanogaster Model Honors Thesis

honors thesis advisor

fiu authors

  • Perez, Laura

abstract

  • Mitochondria act as the powerhouse of eukaryotic cells. These organelles are ultimately able to convert chemical energy from food into ATP through use of the electron transport chain. Dysfunction in the electron transport chain generates reactive oxygen species (ROS), which damage cells and can ultimately lead to their death. Recent work has implicated mitochondrial dysfunction and ROS as a hallmark of several neurodegenerative diseases, including Parkinson’s disease, suggesting a possible contribution to induction of neurodegeneration. The sporadic onset of Parkinson’s disease in the majority of cases raises the possibility that the environment is a significant modulator of mitochondrial function. Nutrient-responsive signaling processes are key regulators of autophagy, a process that recycles aged, malfunctioning mitochondria. To test whether nutrition affects onset of neurodegenerative phenotypes, we tested an established rotenone-induced Drosophila model of Parkinson’s disease. Using a climbing assay, it was found that both yeast and sucrose enhanced the phenotypes cause by the rotenone, yeast more so than sucrose. Mortality was also significantly increased by the yeast supplementation. These results indicate that dietary supplementation enhances neurodegenerative phenotypes, opening the way to investigation of specific signaling mechanisms.

publication date

  • April 17, 2017

keywords

  • Parkinson's Disease
  • drosophila
  • mortality
  • motility
  • nutrition
  • rotenone