**1. Introduction**

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Parkinson disease (PD) is a degenerative disorder of the central nervous system and one of the most common neurologic disorders, affecting approximately 1% of individuals older than 60 years and causing progressive disability that can be slowed, but not halted, by treatment (Poewe, 2006; DeLong & Juncos, 2008). The epidemiology of Parkinson disease is not geneti‐ cally predetermined, but influenced by environmental factors which may be geographically heterogeneousn (Tanner & Langston, 1990). Major gene mutations cause only a small propor‐ tion of all cases and that in most cases; non-genetic factors play a part, probably in interaction with susceptibility genes (de Lau & Breteler, 2006). A number of environmental factors have been associated with an increased risk of Parkinson's including: pesticide exposure, head injuries, and living in the country or farming (Noyce et al. 2012; Van Maele-Fabry et al. 2012). Parkinson disease is characterised by focal loss of melanin –containing neurons of the central and caudal parts of the zona compacta of the substantia nigra (Jellinger 1987). Dopamine deficiency of the nigrostrial system is the hallmark of PD disorder. The cause of the degener‐ ation of the dopamine containing neurons in the substantia nigra of patients with PD is nknown. Excessive free radical production has been suggested as a consequence of the catabolism of the monoamines (Dexter et al 1989). It has been shown those catalase and glutathione peroxidases are reduced in the substantia nigra of PD patients (Sofic et al. 1992). It has therefore been suggested that additional antioxidant therapy ncluding vitamins-E and C may be helpful to slowing the progression of PD. Increasing evidence indicates that PD is primarly a Mitochondrial disorder and thus the use of compounds With good mitochondrial penetrance, (CoQ10), could Potentially be of benefit in this disease (Matthews et al 1998).

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