کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
6021923 | 1580655 | 2014 | 10 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Interleukin-1β mediated amyloid plaque clearance is independent of CCR2 signaling in the APP/PS1 mouse model of Alzheimer's disease
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کلمات کلیدی
bone marrow-derivedCCL2eGFPrAAV2APPswe/PS1dE9AβBMDAPPchemokine (C-C motif) receptor 2IL-1βIBA1CCR2APP/PS1 - APP / PS1FIV - IVFNeuroinflammation - التهاب عصبیInterleukin-1 beta - اینترلوکین-1 بتاInterleukin-1β - اینترلوکین-1βamyloid beta - بتا آمیلوئیدAlzheimer's disease - بیماری آلزایمرionized calcium binding adaptor molecule 1 - مولکول آداپتور اتصال دهنده کلسیم یونیزه 1Monocytes - مونوسیتهاFeline immunodeficiency virus - ویروس نقص ایمنی بچهenhanced green fluorescent protein - پروتئین فلورسنت سبز افزایش یافته استamyloid precursor protein - پروتئین پیش ماده آمیلوئی
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
عصب شناسی
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Interleukin-1β mediated amyloid plaque clearance is independent of CCR2 signaling in the APP/PS1 mouse model of Alzheimer's disease Interleukin-1β mediated amyloid plaque clearance is independent of CCR2 signaling in the APP/PS1 mouse model of Alzheimer's disease](/preview/png/6021923.png)
چکیده انگلیسی
Neuroinflammation is a key component of Alzheimer's disease (AD) pathogenesis. Particularly, the proinflammatory cytokine interleukin-1 beta (IL-1β) is upregulated in human AD and believed to promote amyloid plaque deposition. However, studies from our laboratory have shown that chronic IL-1β overexpression in the APPswe/PSEN1dE9 (APP/PS1) mouse model of AD ameliorates amyloid pathology, increases plaque-associated microglia, and induces recruitment of peripheral immune cells to the brain parenchyma. To investigate the contribution of CCR2 signaling in IL-1β-mediated amyloid plaque clearance, seven month-old APP/PS1/CCR2â/â mice were intrahippocampally transduced with a recombinant adeno-associated virus serotype 2 containing the cleaved form of human IL-1β (rAAV2-IL-1β). Four weeks after rAAV2-IL-1β transduction, we found significant reductions in 6E10 and Congo red staining of amyloid plaques that was confirmed by decreased levels of insoluble Aβ1-42 and Aβ1-40 in the inflamed hippocampus. Bone marrow chimeric studies confirmed the presence of infiltrating immune cells following IL-1β overexpression and revealed that dramatic reduction of CCR2+ peripheral mononuclear cell recruitment to the inflamed hippocampus did not prevent the ability of IL-1β to induce amyloid plaque clearance. These results suggest that infiltrating CCR2+ monocytes do not contribute to IL-1β-mediated amyloid plaque clearance.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neurobiology of Disease - Volume 69, September 2014, Pages 124-133
Journal: Neurobiology of Disease - Volume 69, September 2014, Pages 124-133
نویسندگان
Fátima Rivera-Escalera, Sarah B. Matousek, Simantini Ghosh, John A. Olschowka, M. Kerry O'Banion,