Mitochondria are vitally important organelles involved in an array of functions. The most notable is their prominent role in energy metabolism, where they generate over 90% of our cellular energy in the form of ATP through oxidative phosphorylation. Mitochondria are involved in various other processes including the regulation of calcium homeostasis and stress response. Mitochondrial complex I impairment and subsequent oxidative stress have been identified as modulators of cell death in experimental models of Parkinson's disease (PD). Identification of specific genes which are involved in the rare familial forms of PD has further augmented the understanding and elevated the role mitochondrial dysfunction is thought to have in disease pathogenesis. This paper provides a review of the role mitochondria may play in idiopathic PD through the study of experimental models and how genetic mutations influence mitochondrial activity. Recent attempts at providing neuroprotection by targeting mitochondria are described and their progress assessed. 1. Introduction Parkinson’s disease (PD) is a chronic, progressive neurodegenerative disorder, the second most common age-related neurodegenerative disease after Alzheimer’s disease [1]. It can be characterised clinically by rigidity, resting tremor, and postural instability [2]. These symptoms result from the loss of dopaminergic neurons in the substantia nigra pars compacta (SNpc) and a subsequent depletion of dopamine in the striatum [2]. The etiopathogenesis of PD is still not fully understood. 95% of cases are sporadic: a multifactorial, idiopathic disorder resulting from contributions of environmental and genetic susceptibility. The remaining 5% is the result of genetic mutations, of which there are several types, many only recently identified. However, old age remains the greatest risk factor, with 0.3% of the entire population affected, rising to more than 1% in the over 60？s and 4% in those over the age of 80 [3]. The two forms of PD share pathological, biochemical, and clinical features, with dysfunction of mitochondria and associated molecular pathways representing a bridge between the two forms of PD as well as the natural ageing process. Most mitochondrial dysfunction results from damage to complex I—or NADH (nicotinamide adenine dinucleotide phosphate):ubiquinone oxidoreductase—the first and most complex protein in the electron transport chain [4]. It is a large protein, consisting of 42 or 43 subunits [5] on the inner mitochondrial membrane, which forms part of the oxidative phosphorylation system [6].
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