Introduction/background Parkinson's disease (PD) is the most frequent movement disorder and the second most common neurodegenerative disease (Bueler 2009). Over 1% of the entire population over the age of 60, and up to 5% of those in their 80s, are affected by PD (Wood-Kaczmar, Gandhi et al. 2006). The pathogenesis of Parkinson's disease remains unclear, but can be classified as sporadic, being the most common form, and Mendelian, accounting for 5–10% of all cases of Parkinson's disease (Guo 2008). Studies on the Mendelian onset of Parkinson's disease have led to the identification of five genes linked to this neurodegenerative disease (Guo 2008). α-Synuclein (SNCA) and leucine-rich repeat kinase 2 (LRRK2) mediate autosomal dominant forms of PD. PTEN-induced putative kinase 1 (PINK1), PARKIN, and DJ-1 mediate autosomal recessive forms and have been associated with sporadic cases due to mutations (Dodson and Guo 2007). The clinical symptoms of the sporadic and Mendelian forms are similar and consist of the manifestation of tremors, progressive rigidity, bradykinesia and gait abnormalities (Van Laar and Berman 2009). Progressive dopaminergic (DA) neuronal loss in the substantia nigra, a site primarily responsible for dopamine metabolism and iron content in the brain, is pathologically associated with the first 3 symptoms. Parkinson's disease, however, also affects non-DA neurons in the brain, which can lead patients to experience cases of depression, anxiety, or obsessive-compulsive disorder before the manifestation of motor symptoms (Guo 2008). Current medical treatment of Parkinson's disease focuses on dopamine replacement and unfortunately poorly alleviates the overall symptoms of Parkinson's disease, especially DA-independent symptoms (Guo 2008). The complex pathological mechanism of Parkinson's disease requires new global treatments and... half of the paper ......rogress report 2 dueWeek 10 – Finalization of experimental results and 20 minute seminar talkWorks CitedBueler, H. (2009). “Impaired mitochondrial dynamics and function in the pathogenesis of Parkinson's disease.” Esp Neurol.Deng, H., M.W. Dodson, et al. (2008). “The Parkinson's disease genes pink1 and parkin promote mitochondrial fission and/or inhibit fusion in Drosophila.” Proc Natl Acad Sci USA 105(38): 14503-8. Dodson, M. W. and M. Guo (2007). "Pink1, Parkin, DJ-1, and mitochondrial dysfunction in Parkinson's disease." Curr Opin Neurobiol 17(3): 331-7.Guo, M. (2008). Translational Research BWF.Van Laar, VS and SB Berman (2009). "Mitochondrial dynamics in Parkinson's disease". Esp Neurol.Wood-Kaczmar, A., S. Gandhi, et al. (2006). "Understanding the molecular causes of Parkinson's disease." Mol Med Trends 12(11): 521-8.