کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
6021794 | 1580653 | 2014 | 9 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Altered selenium status in Huntington's disease: Neuroprotection by selenite in the N171-82Q mouse model
دانلود مقاله + سفارش ترجمه
دانلود مقاله ISI انگلیسی
رایگان برای ایرانیان
کلمات کلیدی
mutant huntingtin proteinmHTTGSHGSSGhttDARPP32Förster resonance energy transfer - انتقال انرژی تابشی ForsterFRET - انتقال انرژی رزونانسی فورسترAlzheimer's disease - بیماری آلزایمرHuntington's disease - بیماری هانتینگتونNeurodegeneration - تولید نوروژنیکDiet - رژیم غذاییSelenoprotein - سلنوپروتئینSelenium - سلنیومICP-MS - طیفسنجی جرمی پلاسمای جفتشده القاییNeuroprotection - محافظت نورونی یا محافظت از عصبhuntingtin protein - پروتئین huntingtinGlutathione - گلوتاتیونoxidized glutathione - گلوتاتیون اکسید شده
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
عصب شناسی
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Altered selenium status in Huntington's disease: Neuroprotection by selenite in the N171-82Q mouse model Altered selenium status in Huntington's disease: Neuroprotection by selenite in the N171-82Q mouse model](/preview/png/6021794.png)
چکیده انگلیسی
Disruption of redox homeostasis is a prominent feature in the pathogenesis of Huntington's disease (HD). Selenium an essential element nutrient that modulates redox pathways and has been reported to provide protection against both acute neurotoxicity (e.g. methamphetamine) and chronic neurodegeneration (e.g. tauopathy) in mice. The objective of our study was to investigate the effect of sodium selenite, an inorganic form of selenium, on behavioral, brain degeneration and biochemical outcomes in the N171-82Q Huntington's disease mouse model. HD mice, which were supplemented with sodium selenite from 6 to 14 weeks of age, demonstrated increased motor endurance, decreased loss of brain weight, decreased mutant huntingtin aggregate burden and decreased brain oxidized glutathione levels. Biochemical studies revealed that selenite treatment reverted HD-associated changes in liver selenium and plasma glutathione in N171-82Q mice and had effects on brain selenoprotein transcript expression. Further, we found decreased brain selenium content in human autopsy brain. Taken together, we demonstrate a decreased selenium phenotype in human and mouse HD and additionally show some protective effects of selenite in N171-82Q HD mice. Modification of selenium metabolism results in beneficial effects in mouse HD and thus may represent a therapeutic strategy.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neurobiology of Disease - Volume 71, November 2014, Pages 34-42
Journal: Neurobiology of Disease - Volume 71, November 2014, Pages 34-42
نویسندگان
Zhen Lu, Eileen Marks, Jianfang Chen, Jenna Moline, Lorraine Barrows, Merl Raisbeck, Irene Volitakis, Robert A. Cherny, Vanita Chopra, Ashley I. Bush, Steven Hersch, Jonathan H. Fox,