کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
9191873 | 1186603 | 2005 | 12 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Oxidative stress and inflammation in Parkinson's disease: is there a causal link?
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کلمات کلیدی
4-hydroxy-2,3-nonenaldihydroxyphenylacetaldehydeGSHCOX-2HNEMAOiNOSeNOSIFN-γLPSDOPACMPP+ - MPP +inducible NOS - NOS قابل القاییendothelial NOS - اندوتلیال NOSinterferon-gamma - اینترفرون گاماinterleukin - اینترلوکینCNS - دستگاه عصبی مرکزیdihydroxyphenylacetic acid - دی هیدروکسی فنیل اسیدهای اسیدcentral nervous system - سیستم عصبی مرکزیCyclooxygenase-2 - سیکلوکوکسیژناز2monoamine oxidase - مونوآمین اکسیدازها Glutathione - گلوتاتیون
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
عصب شناسی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Parkinson's disease (PD) is a neurodegenerative disorder characterized by a dramatic loss of dopaminergic neurons in the substantia nigra (SN). Among the many pathogenic mechanisms thought to contribute to the demise of these cells, dopamine-dependent oxidative stress has classically taken center stage due to extensive experimental evidence showing that dopamine-derived reactive oxygen species and oxidized dopamine metabolites are toxic to nigral neurons. In recent years, however, the involvement of neuro-inflammatory processes in nigral degeneration has gained increasing attention. Not only have activated microglia and increased levels of inflammatory mediators been detected in the striatum of deceased PD patients, but a large body of animal studies points to a contributory role of inflammation in dopaminergic cell loss. Recently, postmortem examination of human subjects exposed to the parkinsonism-inducing toxin, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), revealed the presence of activated microglia decades after drug exposure, suggesting that even a brief pathogenic insult can induce an ongoing inflammatory response. Perhaps not surprisingly, non-steroidal anti-inflammatory drugs (NSAIDs) have been shown to reduce the risk of developing PD. In the past few years, various pathways have come to light that could link dopamine-dependent oxidative stress and microglial activation, finally ascribing a pathogenic trigger to the chronic inflammatory response characteristic of PD.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Experimental Neurology - Volume 193, Issue 2, June 2005, Pages 279-290
Journal: Experimental Neurology - Volume 193, Issue 2, June 2005, Pages 279-290
نویسندگان
Andreas Hald, Julie Lotharius,