Johns Hopkins University

To whom correspondence should be addressed. E-mail : ylee69(at).jhmi.edu

Parkinson's disease (PD) is the most common neurological movement disorder characterized by the dysfunctional nigrostriatal dopaminergic pathway majorly due to the progressive loss of dopamine producing neurons in the substantia nigra pas compacta (SNpc) of midbrain. The degeneration in this circuit is responsible for PD-linked clinical symptoms of movement deficit including slow movement, tremor, rigidity and postural instability because dopamine transmission in nigrostriatal pathway is crucial in controlling muscle movement and balance. Besides, the progressive loss of motor control is often accompanied by secondary non-motor symptoms which are associated with PD and sometimes more debilitating to the affected patients. They include pain, constipation, depression, anxiety, dementia and sweating. In the degenerating environment of SN, intracellular protein deposits, termed Lewy bodies, which are majorly composed of α-synuclein (α-syn), are easily found and indeed used as a pathological hallmark for PD (Lang and Lozano 1998; Lang and Lozano 1998). Considering the prevalence of disease, with more than 1 million people affected in North America with ever increasing rate due to extended lifespan (Lang and Lozano 1998), and no cure except for the anti-symptomatic medications of dopamine supplementation (i.e., L-DOPA plus carbidopa regimen), it cannot be more emphasized to understand the underlying mechanisms by which the degeneration and biochemical alterations are initiated and progress, which can ultimately prompt the development of therapeutic strategies. Since we have ponderous background knowledge about the functions of genes which are linked to PD in cell system and in vitro (Moore, West et al. 2005), the next step and focus should be given to validating the pathways in in vivo mouse system and further testing potential chemicals or disease modifying genes in PD animal model.

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