کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8965855 | 1646745 | 2018 | 31 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
A low blood copper concentration is a co-morbidity burden factor in Parkinson's disease development
ترجمه فارسی عنوان
غلظت مس کم خون یکی از عوامل باردهی در بیماری پارکینسون است
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کلمات کلیدی
IL-6Hoehn and Yahr stageSOD3CSIMMSEUPDRSBDIPPDPIGDCeruloplasminH&Y - H & YROS - ROSSNpc - SNPCinterleukin-6 - اینترلوکین ۶Frontal assessment battery - باتری ارزیابی جلوParkinson’s disease - بیماری پارکینسونFab - فابMini-Mental State Examination - معاینه دولتی مینی روانشناسیHospital Anxiety and Depression Scale - مقیاس اضطراب و افسردگی بیمارستانUnified Parkinson’s Disease Rating Scale - مقیاس درجه بندی بیماری بیماری پارکینسون متحدHADS - هاتReactive oxygen species - گونههای فعال اکسیژن
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
چکیده انگلیسی
Parkinson's disease (PD) patients are often characterized by copper dyshomeostasis, which is responsible for ROS formation and fibrillogenesis. However, the relationships between copper metabolism and PD development are unclear. In this study in 50 patients with PD (pPD) and 50 age-matched healthy individuals, the serum total copper concentration, oxidase activity, ceruloplasmin and SOD3 protein concentrations were measured; and amount of copper atoms per ceruloplasmin molecule was calculated. These parameters were lower in pPD relatively to healthy volunteers. Decrease in concentrations of SOD3, ceruloplasmin, and copper but increase of interleukin-6 levels were associated with a risk of PD. Two consistent patterns were identified. First, a low serum copper concentration related with PD development and predominantly affected the non-motor symptoms of PD. There was no correlation between copper concentration and ceruloplasmin oxidase activity level (râ¯=â¯0.27) in pPD. Second, Chelex 100 treatment revealed that pPD ceruloplasmin compared with ceruloplasmin of healthy individuals displayed smaller content of labile copper atoms. The presence or absence of these atoms had no effect on ceruloplasmin enzymatic activities. Our findings suggest that cuproenzyme deficiency, which is typical for PD, can be caused by violation of metabolic incorporation of the labile copper atoms into ceruloplasmin molecule.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience Research - Volume 135, October 2018, Pages 54-62
Journal: Neuroscience Research - Volume 135, October 2018, Pages 54-62
نویسندگان
Ekaterina Y. Ilyechova, Irina V. Miliukhina, Iurii A. Orlov, Zamira M. Muruzheva, Ludmila V. Puchkova, Marina N. Karpenko,