Mitochondria are the main suppliers of ATP in most mammalian cells, it control both neurotic and the apoptosis signaling pathway, which is the apoptotic cell death pathways. Mitochondria is associated with the coordination of the cellular calcium (Ca2+) signaling. Mitochondria also produces and are targets of free radical species that control many characteristics of the cell’s physiology, this can be seen in Figure 1 and the structure and function can be seen in Figure 2. (Duchen and Szabadkai 2010)
Currently, the theory that persists is that mitochondria is the progeny of aerobic bacteria that colonized a prokaryote (Spees, et al. 2006). Mitochondria has DNA, (mtDNA) which are not protected by the histones as in the nuclear DNA (Croteau and Bohr 1997). In the nuclear DNA, the histones offers a shielding to protect the DNA from damaging the free radicals (Milligan, Aguilera and Ward 1993), it is also required to repair the double stranded DNA breaks (Celeste, et al. 2003). The mitochondrial DNA on the other had is lacking the histones, hence
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Mitochondrial dysfunction plays a key role in the pathogenesis of the Parkinson’s disease. Deficiencies of the mitochondrial complex I is associated with the Parkinson’s disease. The genetic defects in proteins such as α- synuclein, Parkin, DJ-1, PINK1 (PTEN- induced putative kinase 1) and LRRK2 (leucine- rich repeat kinase 2) also HTRA2/OMI are all proteins associated with Parkinson’s disease (Lees, Hardy and Revesz 2009). These proteins are therefore associated with the mitochondria and they form part of the cascade of the related interacting proteins. Heterozygous missense mutations in HTRA2/OMI has been found in the “random” cases of Parkinson’s disease. HtrA2 is homologous with bacterial Deg proteases, localizes to the mitochondrial intermembrane space where it protects against mitochondrial