**5. Conclusions**

Parkinson's disease is characterized by persistent, coordinated, nuclear-encoded cellular energy defects to which nigral dopamine neurons are intrinsically more susceptible than others cells. Complex I dysfunction in PD may be a biochemically detectable "tip of the iceberg" of a deeper molecular defect comprising the entire nuclear-encoded electron transfer chain. Under expression of PGC-1α-controlled genes involved in cellular energetic might represent a common link for these diverse manifestations of defects in mitochondrial biogenesis, and abnormal glucose utilization. One of the basic postulates of the mitochondrial theory of aging and neurodegenerative diseases is that there is a significant reduction in the capacity for ATP production in the brain and other organs of old mammals. The concept of a decrease in the effectiveness of the mitochondrial process of energy transduction (or oxidative phosphorylation) is expressed as an under function of "the mitochondrial redox-energy axis" (Yap et al., 2010). Although mitochondrial complexes, complex I (Valdez et al., 2004; Boveris & Navarro, 2008; Navarro et al., 2009), complex IV (Valdez et al., 2004; Boveris & Navarro, 2008), and complex V (Lam et al., 2009), are considered the main targets in neurodegeneration and aging, there are also cytosolic enzymes whose activities are simultaneously decreased, such as succinyl-CoA-transferase (Lam et al. 2009) and as 6-phosphofructo-2-kinase (Herrero-Mendez et al., 2009). The cytosolic-mitochondrial interaction is certainly affected and there is recognition of a depressed glucose metabolism as the earliest and consistent abnormality in neurodegenerative diseases (Yap et al., 2009).
