| Parkinson's disease is characterized by the progressive loss of dopamine (DA) in the caudate nucleus, putamen, and substantia nigra upon the loss of dopaminergic neurons in the substantia nigra pars compacta (SNpc), resulting in cardinal motor symptoms such as tremor at rest, bradikinesia, muscular rigidity, stooped posture, and instability[1].The evidence for a chronic inflammatory reaction in the brain is particularly strong in Alzheimer's disease (AD) where it has been extensively studied, but there is also a considerable literature suggesting that a local immune reaction occurs in affected regions of the brain in Parkinson's disease (PD). The large number of recent reviews on the subject bears witness to the growing realization of the possible importance of this inflammatory response to PD progression[2]. The role of immune mechanisms in neurodegenerative diseases such as PD is an important area of investigation. Death of, or injury to, neurons leads to activation of glia and production of many pro-inflammatory cytokines and molecules[3].The complement system plays a key role in immune reactions and can kill host tissue directly by activation of membrane attack complex (MAC), or indirectly, through activation of macrophages that produce abundant levels of oxygen radicals and other toxic products. In PD, components of complement have been demonstrated in Lewy bodies, indicating activation of the classic complement pathway[4] [5]. Moreover, serum from patients with PD has been shown to be toxic to mesencephalic neurons in culture, and this toxicity is mediated by complement activation[6]. However, so far, there is still no in vivo studies demonstrating whether C3 plays a role in the pathogenesis of PD or in any animal models of PD.Recent studies demonstrated that low dose whole body irradiation is able to confer...
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