SELECTIVE DEGENERATION OF DOPAMINERGIC NEURONS IN DROSOPHILA MODELS OF PARKINSON'S DISEASE
Kiara Andrades1, Mehmet Enes Inam1, Antonio Tito Jr.2, Sheng Zhang2, Hugo Bellen3, Shebna Cheema1.
1University of Houston Downtown, Houston, TX, 2University of Texas-Health Science Center Houston, TX, 3Baylor College of Medicine, Houston, TX.
Parkinson’s disease (PD) is the most common neurodegenerative movement disorder that is caused by the degeneration of dopamine neurons in the substantia nigra of the mesencephalon. The cause of degeneration of dopamine neurons is still unknown. We utilized Drosophila melanogaster as a model organism due to its low cost and unlimited number of test subjects. The homologs for these genes in Drosophila do not contribute to age-dependent neural degeneration. In Drosophila, PARK2 is involved in removing dysfunctional proteins and directing them to the proteasome system for further degradation. Parkin mutation in Drosophila leads to the disruption of mitochondria, which cause the accumulation of toxic-free reactive oxygen species (ROS). Parkin mutation along with wildtype were used to determine changes in the number of dopaminergic neurons of the aging adult brains of Drosophila. Results show no remarkable changes in the number of DA neurons due to aging. Thus, we further determined the non-autonomous contribution of glial cells in the viability of dopamine neurons. As a spontaneously toxic molecule, DA is protected from auto-oxidation by β-alanine insertion mediated by ebony in the glial cells. Thus, a fly line containing parkin and ebony recombination was generated. This study provides the first insight into the role of glial cells in the viability of dopamine neurons in a genetic model of Parkinson’s disease.