2006
DOI: 10.1007/s10571-006-9061-9
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Cellular and Molecular Mechanisms of Parkinson’s Disease: Neurotoxins, Causative Genes, and Inflammatory Cytokines

Abstract: 1. Parkinson's disease (PD) is considered to be an aging-related neurodegeneration of catecholamine (CA) systems [typically A9 dopamine (DA) neurons in the substantia nigra and A6 noradrenaline (NA) neurons in the locus coeruleus]. The main symptom is movement disorder caused by a DA deficiency at the nerve terminals of fibers that project from the substantia nigra to the striatum. Most PD is sporadic (sPD) without any hereditary history. sPD is speculated to be caused by some exogenous or endogenous substance… Show more

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Cited by 107 publications
(80 citation statements)
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“…Intensive studies have revealed that several molecular and cellular events, including oxidative stress, mitochondrial dysfunction, proapoptotic mechanisms, and abnormal protein handling, might be involved in the pathogenesis of PD (Nagatsu and Sawada, 2006). However, the mechanisms underlying the neuronal loss in PD are not fully understood.…”
Section: Introductionmentioning
confidence: 99%
“…Intensive studies have revealed that several molecular and cellular events, including oxidative stress, mitochondrial dysfunction, proapoptotic mechanisms, and abnormal protein handling, might be involved in the pathogenesis of PD (Nagatsu and Sawada, 2006). However, the mechanisms underlying the neuronal loss in PD are not fully understood.…”
Section: Introductionmentioning
confidence: 99%
“…The cardinal clinical symptoms of PD include dyskinesia, resting tremor, rigidity, and gait disturbance. Current therapeutic interventions are limited to alleviating the symptoms of PD, and they fail to halt the progression of neurodegeneration (Gao et al, 2003a).Although oxidative stress, mitochondrial dysfunction, excitotoxicity, and apoptotic processes have been identified as being involved in neuronal degeneration (Nagatsu and Sawada, 2006), the mechanisms responsible for the progressive feature of neurodegeneration are not fully understood. In recent years, increasing evidence has strongly suggested that neuroinflammation is an important contributor to the pathogenesis of neurodegenerative diseases, such as PD, Alzheimer's disease, and multiple sclerosis.…”
mentioning
confidence: 99%
“…Although oxidative stress, mitochondrial dysfunction, excitotoxicity, and apoptotic processes have been identified as being involved in neuronal degeneration (Nagatsu and Sawada, 2006), the mechanisms responsible for the progressive feature of neurodegeneration are not fully understood. In recent years, increasing evidence has strongly suggested that neuroinflammation is an important contributor to the pathogenesis of neurodegenerative diseases, such as PD, Alzheimer's disease, and multiple sclerosis.…”
mentioning
confidence: 99%
“…Inflammation associated with PD can be initiated in the brain by internal factors such as a brain injury, a genetic mutation or some other brain insult or dysfunction (Nagatsu and Sawada 2006;Tansey, McCoy et al 2007;Hirsch and Hunot 2009;Qian, Flood et al 2010) (Figure 1). These sorts of intracerebral inflammatory stimuli activate the microglia which then up-regulate production of inflammatory factors including inflammatory cytokines such as TNFα, IL-1β or IL-6, as well as NO and ROS Nagatsu and Sawada 2006;Tansey, McCoy et al 2007).…”
Section: Proposed Model Of Neuroinflammation In Pdmentioning
confidence: 99%
“…Expression of the inflammatory markers MHC II, TNFα and cyclooxygenase (COX-2) is also higher in SN tissue of patients with PD than in comparable tissue from unaffected controls (McGeer, Itagaki et al 1988;Boka, Anglade et al 1994;Knott, Stern et al 2000). Additionally, levels of proinflammatory mediators, including TNFα, IL-1β, IL-6, (ROS), and eicosanoids, are all elevated in the SN, striatum, cerebrospinal fluid (CSF) and/or peripheral blood mononuclear cells (PBMC) of PD patients (McGeer, Itagaki et al 1988;Qureshi, Baig et al 1995;Mogi, Harada et al 1996;Imamura, Hishikawa et al 2003;Teismann and Schulz 2004;Nagatsu and Sawada 2006;Sawada, Imamura et al 2006;Hirsch and Hunot 2009;Pisani, Moschella et al 2010). Nitric oxide (NO) free radicals are also elevated in PD as indicated by increased nitrite (an indicator for NO) present in the CSF, as well as increased expression of inducible nitric oxide synthase (iNOS) within the SN of PD patients (Qureshi, Baig et al 1995).…”
mentioning
confidence: 99%