کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
329547 1433667 2006 10 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Differences in the early inflammatory responses to toxin-induced demyelination are associated with the age-related decline in CNS remyelination
موضوعات مرتبط
علوم زیستی و بیوفناوری بیوشیمی، ژنتیک و زیست شناسی مولکولی سالمندی
پیش نمایش صفحه اول مقاله
Differences in the early inflammatory responses to toxin-induced demyelination are associated with the age-related decline in CNS remyelination
چکیده انگلیسی

CNS remyelination occurs more rapidly in young adult rats than in old rats. Since the inflammatory response initiated by demyelination is an important trigger for remyelination, we address whether ageing changes in remyelination are associated with changes in the inflammatory response. Using a toxin model of demyelination, where the inflammatory response largely comprises macrophages, we show that there is a delay in both recruitment and activation of OX-42+ and macrophage scavenger receptor B+ macrophages following demyelination in older rats (10–13 months) compared to young rats (8–10 weeks). This difference is associated with a slower onset of increased expression of several chemokine mRNAs. However, many inflammatory cytokines have similar mRNA expression patterns, with the exception of IL-1β, IL-6 and TNF-α, which have prolonged expression in the older animals. Differences in IL-1β mRNA expression, a cytokine specifically implicated in CNS remyelination, are not reflected in differences in protein expression detected by immunocytochemistry. These data relate the age-associated delay in remyelination efficiency to changes in the macrophage and inflammatory mediator response to demyelination.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neurobiology of Aging - Volume 27, Issue 9, September 2006, Pages 1298–1307
نویسندگان
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