Green tea catechin, EGCG, modulates mitochondrial dynamics in dopaminergic neurons of α-synuclein transgenic flies resulting in mobility improvement.

• Main Author: Choo, Wen Rui.
• Other Authors: School of Biological Sciences
• Format: Final Year Project
• Language: English
• Published: 2012
• Subjects: DRNTU::Science
• Online Access: http://hdl.handle.net/10356/50655
• Institution: Nanyang Technological University

Parkinson’s disease (PD) is characterized pathologically by the hallmark presence of Lewy bodies, which are intraneuronal inclusions comprised of chiefly α-synuclein. Studies have illustrated an association between the toxicity induced by over-expression of α-synuclein and PD-related locomotive deficiency, but specific mechanisms remains unclear. In this study we observed intriguing lost of climbing abilities that is void of apparent DA neuronal loss in wild-type and mutant α-synuclein, A30P and A53T, transgenic PD flies. Using a mitochondrial-targeting sequence tagged Green fluorescence protein reporter (mito-GFP), we observed aberrant mitochondria dynamics in A30P and A53T flies, rendering their neuronal mitochondrial sizes significantly smaller than comparative control. Results thus suggest that, contrary to conventional belief, DA neuron functional loss instead of overt DA neuronal loss actually accounts for the presentation of PD-associated locomotive dysfunction. Furthermore, we have demonstrated that Epigallocatechin 3-gallate (EGCG), a polyphenol found in Green tea, is able to improve locomotive defects and restore DA neuronal loss through modulation of neuronal mitochondrial dynamics.