کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
9989767 | 1580765 | 2005 | 7 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Differential effects of oligomeric and fibrillar amyloid-β1-42 on astrocyte-mediated inflammation
دانلود مقاله + سفارش ترجمه
دانلود مقاله ISI انگلیسی
رایگان برای ایرانیان
کلمات کلیدی
Amyloid-β (Aβ)Astrocyte - آستروسیتinflammation - التهاب( توروم) Interleukin-1β (IL-1β) - اینترلوکین 1β (IL-1β)Alzheimer's disease - بیماری آلزایمرInducible nitric oxide synthase (iNOS) - سنتاز اکسید نیتریک قابل انعطاف (iNOS)Tumor necrosis factor-α (TNF-α) - عامل نکروز تومور-α (TNF-α)Nitric oxide (NO) - نیتریک اکسید (NO)
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
عصب شناسی
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Differential effects of oligomeric and fibrillar amyloid-β1-42 on astrocyte-mediated inflammation Differential effects of oligomeric and fibrillar amyloid-β1-42 on astrocyte-mediated inflammation](/preview/png/9989767.png)
چکیده انگلیسی
Activated glia, as a result of chronic inflammation, are associated with amyloid-β peptide (Aβ) deposits in the brain of Alzheimer's disease (AD) patients. In vitro, glia are activated by Aβ inducing secretion of pro-inflammatory molecules. Recent studies have focused on soluble oligomers (or protofibrils) of Aβ as the toxic species in AD. In the present study, using rat astrocyte cultures, oligomeric Aβ induced initial high levels of IL-1β decreasing over time and, in contrast, fibrillar Aβ increased IL-1β levels over time. In addition, oligomeric Aβ, but not fibrillar Aβ, induced high levels of iNOS, NO, and TNF-α. Our results suggest that oligomers induced a profound, early inflammatory response, whereas fibrillar Aβ showed less increase of pro-inflammatory molecules, consistent with a more chronic form of inflammation.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neurobiology of Disease - Volume 18, Issue 3, April 2005, Pages 459-465
Journal: Neurobiology of Disease - Volume 18, Issue 3, April 2005, Pages 459-465
نویسندگان
Jill A. White, Arlene M. Manelli, Kristina H. Holmberg, Linda J. Van Eldik, Mary Jo LaDu,