الفهرس 
INTRODUCTIONOnly 14 pages are availabe for public view
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Abstract
PD is a progressive neurodegenartive disorder defined by a characteristic clinical syndrome of bradykinesia, tremor, rigidity, and postural instability. PD is currently regarded as the most common degenerative disorder of the aging brain after the Alzheimer’s disease with extremely high psychosocial impacts and noticeable declines in patients’ quality of life. The cardinal biochemical abnormality in PD is the profound deficit in brain dopamine level attributed to the loss of neurons of the nigrostriatal dopaminergic pathway. This pathway is made of dopaminergic neurons whose cell bodies are located in SNC and whose axons and nerve terminals project to the striatum.
Free radical–mediated injury has been suggested as and continues to be, the main hypothesis for pathogenesis of neural degeneration in PD. Mitochondria have been claimed as dominant sites for oxidative stress-driven initiation and propagation in PD. Defective mitochondrial CI function is observed in the substantia nigra of PD brains.
A recent study has demonstrated that α-Synculein monomers and oligomers associate with the inner mitochondrial membrane where they can physically bind to CI, thereby interfering with mitochondrial function and increasing free radicals production Indeed , the exact pathogenic mechanism leading to neurodegeneration in PD is not fully understood. However, it is assumed that cell death occurs by way of a signal-mediated apoptotic process. Mitochondrial defects in PD in particular can be closely linked to apoptosis as reduced levels of complex I can cause impaired proton pumping, reduced mitochondrial membrane potential, and increased mitochondrial membrane permeability with the release of apoptosis-initiating factors.