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Parkinsons Essay

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Introduction:
A broad spectrum of neurodegenerative diseases of aging are associated with chronic inflammation, including diseases that affect the CNS such as Alzheimer’s disease, Parkinson’s disease, amyotrophic lateral sclerosis, and all of the tauopathies, and age-related macular degeneration (Block and Hong, 2005; McGeer et al., 2005). Parkinson’s disease (PD) is the most common neurodegenerative movement disorder (Schapira, 2009a). It is an age-dependent disease characterized by resting tremor, slowed movement, postural instability and muscle rigidity (Gelb et al., 1999). The most prominent pathological features are the severe loss of dopaminergic neurons in the substantia nigra (SN) and the presence of proteinaceous inclusions called Lewy bodies (LBs) primarily composed of fibrillar a-synuclein and ubiquitinated proteins within some remaining nigral neurons (Lees et al., 2009). The recent identification of mutations in several genes linked to rare inherited forms of PD has led to speculation that these mutations promote inclusion formation, ubiquitin-proteosome system (UPS) dysfunction and nigral cell loss, although the precise molecular mechanisms are unclear and the pathology in humans and animal models bearing these mutations is highly variable (Bonifati, 2007; Lim and Ng, 2009). Nevertheless, recent studies of transgenic animals with mutations linked to parkinsonism as well as neurotoxin and virus-based animal models of PD have provided valuable insight into potential pathogenic mechanisms involving neuroinflamation. Human clinical imaging, postmortem examinations and epidemiological studies have recently highlighted the role of neuroinflammation in PD and raise the interesting possibility that chronic inflammation may act as an environmental stressor to promote progressive degeneration of dopaminergic neurons. In the past 15 years, a wealth of new information has emerged to suggest that inflammation derived oxidative stress and cytokine-dependent...

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