کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8686381 | 1580606 | 2018 | 19 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
NLRP3-dependent synaptic plasticity deficit in an Alzheimer's disease amyloidosis model in vivo
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کلمات کلیدی
IL-1EPSPss.c.intracerebroventricularlyIL-1RAHFSPS1i.c.v.APPi.p.Aβpresenilin 1 - Presenilin 1IL-1 receptor antagonist - آنتاگونیست گیرنده IL-1NLRP3 inflammasome - التهاب NLRP3Interleukin-1β - اینترلوکین-1βamyloid beta - بتا آمیلوئیدAlzheimer's disease - بیماری آلزایمرhigh frequency stimulation - تحریک فرکانس بالاTransgenic - تراریختهlong-term potentiation - تقویت درازمدتLTP - تقویت طولانی مدت یا LTP Intraperitoneally - داخل صفاقیsubcutaneously - زیر جلدیwild type - نوع وحشیexcitatory postsynaptic potentials - پتانسیل های پست پراکنده تحریک پذیرamyloid precursor protein - پروتئین پیش ماده آمیلوئی
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
عصب شناسی
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چکیده انگلیسی
Pro-inflammatory mechanisms have recently emerged as an important component of early Alzheimer's disease (AD) pathogenesis. A particularly attractive therapeutic strategy is to selectively prevent the disruptive effects of activation of the innate immune system in the brain at an early transitional stage by reducing the production or directly neutralizing pro-inflammatory cytokines, in particular IL-1β and TNF-α. Here we tested their in vivo effects on synaptic plasticity deficits, which provide sensitive and robust measures of synaptic failure, in a rat model of AD amyloidosis. Using electrophysiological techniques we longitudinally studied the effects of the NLRP3 inflammasome inhibitor Mcc950, the IL-1 receptor antagonist (anakinra) and an anti-TNF-α agent (etanercept) in awake freely moving transgenic rats overexpressing AD associated β-amyloid precursor protein at a pre-plaque stage of amyloidosis. Repeated treatment with Mcc950 reversibly abrogated the inhibition of long-term potentiation. The IL-1 receptor antagonist and etanercept also had a similar beneficial effect on the deficit in synaptic plasticity. Our findings support the clinical development of Mcc950 and clinically available IL-1- and TNF-α-neutralizing agents in early AD.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neurobiology of Disease - Volume 114, June 2018, Pages 24-30
Journal: Neurobiology of Disease - Volume 114, June 2018, Pages 24-30
نویسندگان
Yingjie Qi, Igor Klyubin, A. Claudio Cuello, Michael J. Rowan,