کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
9194734 1580506 2005 8 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
CD40L deletion delays neuronal death in a model of neurodegeneration due to mild impairment of oxidative metabolism
موضوعات مرتبط
علوم زیستی و بیوفناوری ایمنی شناسی و میکروب شناسی ایمونولوژی
پیش نمایش صفحه اول مقاله
CD40L deletion delays neuronal death in a model of neurodegeneration due to mild impairment of oxidative metabolism
چکیده انگلیسی
Inflammatory/immune processes are important in the pathogenesis of neurodegenerative diseases. Thiamine deficiency (TD) models the region selective neuronal loss in brain that accompanies mild impairment of oxidative metabolism. TD induces well-defined alterations in neurons, microglia, astrocytes, and endothelial cells. To test the role of inflammatory/immune mechanisms in TD-induced neurodegeneration, the temporal profile of neurodegeneration was compared to the activation of CD68-positive microglia and ICAM-1-positive endothelial cells during TD in wild type mice and in CD40L−/− mice. CD40L−/− delayed the onset of TD-induced neuronal death as well as the activation of microglia and endothelial cells. The current results suggest that CD40L-mediated immune and inflammatory responses have a role in TD-induced neuronal death.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Journal of Neuroimmunology - Volume 164, Issues 1–2, July 2005, Pages 85-92
نویسندگان
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