Introduction/backgroundParkinson's disease (PD) is the most common movement disorder and the second most common neurodegenerative disease (Bueler 2009). More than 1% of the entire population aged over 60 and up to 5% of those aged 80 are affected by Parkinson's disease (Wood-Kaczmar, Gandhi et al. 2006). The pathogenesis of PD remains unclear, but can be classified as sporadic, being the most common form, and Mendelian, which accounts for 5–10% of all PD cases (Guo 2008). Studies on the Mendelian onset of PD 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) are involved in autosomal dominant forms of Parkinson's disease. Putative PTEN-induced kinase 1 (PINK1), PARKIN and DJ-1 are involved in autosomal recessive forms and have been associated with sporadic cases due to mutations (Dodson and Guo 2007). The clinical symptoms of sporadic and Mendelian forms are similar and consist of the manifestation of tremor, 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 brain iron content, is pathologically associated with the first 3 symptoms. However, PD also affects non-DA neurons in the brain, which may cause patients to experience depression, anxiety, or obsessive-compulsive disorder before the manifestations of motor symptoms (Guo 2008). Current medical treatment of PD focuses on dopamine replacement and unfortunately poorly alleviates overall PD symptoms, particularly AD-independent symptoms (Guo 2008). The complex disease mechanism of PD requires that new comprehensive treatments and...... middle of article ......progress report 2 dueWeek 10 – Finalization of experimental results and 20-minute seminar speechWorks CitedBueler , H. (2009). “Altered mitochondrial dynamics and function in the pathogenesis of Parkinson’s disease.” Exp Neurol. Deng, H., MW Dodson et al. (2008). "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, MW 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). BWF translational research. Van Laar, VS and SB Berman (2009). “Mitochondrial dynamics in Parkinson’s disease.” Exp Neurol. Wood-Kaczmar, A., S. Gandhi, et al. (2006). “Understanding the molecular causes of Parkinson’s disease.” Trends Mol Med 12(11): 521-8.