کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
10958509 1100077 2005 8 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Amyloid-β fibril formation is not necessarily required for microglial activation by the peptides
موضوعات مرتبط
علوم زیستی و بیوفناوری بیوشیمی، ژنتیک و زیست شناسی مولکولی بیولوژی سلول
پیش نمایش صفحه اول مقاله
Amyloid-β fibril formation is not necessarily required for microglial activation by the peptides
چکیده انگلیسی
There is increasing evidence that microglial activation has pathogenic influence on Alzheimer's disease. According to in vitro studies, microglia activated by amyloid-β (Aβ) peptides have been reported to damage or kill neurons by the release of neurotoxic molecules such as tumor necrosis factor-α (TNF-α), interleukin-1β, nitric oxide or reactive oxygen species. Although the relationship between the aggregational state of Aβ peptides and their neurotoxic activities has been well investigated, little is known about the relationship between the aggregational state of Aβ peptides and their ability to induce microglial activation. In the present study, we thus performed both structural and biochemical studies to clarify the relationship between the aggregational state of Aβ peptides and their ability to activate microglia. Our results have shown that, in the presence of interferon-γ, the Aβ25-35(M35Nle) peptide had almost the same potency of activating microglia and producing TNF-α as the Aβ25-35 peptide on both protein and mRNA levels, in spite of the fact that former peptide represented much less amyloid fibril formation than the latter in a thioflavine-T fluorometric assay. These results suggest that Aβ fibril formation is not necessarily required for microglial activation by the peptides.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neurochemistry International - Volume 47, Issue 5, October 2005, Pages 369-376
نویسندگان
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