کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
6273646 | 1614799 | 2014 | 8 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Lixisenatide rescues spatial memory and synaptic plasticity from amyloid β protein-induced impairments in rats
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کلمات کلیدی
Tris-buffered saline containing 0.05% Tween-20DPPIVPPFAβT2DMGLP-1RGSK3βTBSTMWMGLP-1fEPSPs - fEPSP هاamyloid β-protein - β-پروتئین آمیلوئیدamyloid β - آمیلوئید βSprague Dawley - اسپراگ داولیAlzheimer’s disease - بیماری آلزایمرanalysis of variance - تحلیل واریانسANOVA - تحلیل واریانس Analysis of variancepaired-pulse facilitation - تسکین زوایای پالسیlong-term potentiation - تقویت درازمدتLTP - تقویت طولانی مدت یا LTP Type 2 diabetes mellitus - دیابت نوع دوBlood–brain barrier - سد خونی مغزیBBB - سد خونی مغزیLixisenatide - لیکسسناتیدMorris water maze - ماز آب آب موریسSEM - مدل معادلات ساختاری / میکروسکوپ الکترونی روبشیfield excitatory postsynaptic potentials - پتانسیل پستنیپتیک تحریک پذیری میدانglucagon-like peptide-1 - پپتید 1-گلوکاگون-مانندGlycogen synthase kinase 3β - گلیکوزین سنتاز کیناز 3βGLP-1 receptor - گیرنده GLP-1
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
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چکیده انگلیسی
Alzheimer's disease (AD) is a progressive and degenerative disorder accompanied by cognitive impairment, but effective strategies against AD are currently not available. Interestingly, glucagon-like peptide-1 (GLP-1) used in type 2 diabetes mellitus (T2DM) has shown neuroprotective effects in preclinical studies of AD. Lixisenatide, an effective GLP-1 receptor (GLP-1R) agonist with much longer half life than GLP-1, has been licensed in the EU as a treatment for T2DM. However, the neuroprotective effects of lixisenatide in the brain remain to be clarified. In the present study, we report for the first time the effects of lixisenatide on the amyloid β (Aβ) protein-induced impairments in spatial learning and memory of rats, and investigated its electrophysiological and molecular mechanisms. We found that: (1) bilateral intrahippocampal injection of Aβ25-35 resulted in a significant decline in spatial learning and memory of rats, as well as a suppression of in vivo hippocampal long-term potentiation (LTP); (2) lixisenatide treatment effectively prevented the Aβ25-35-induced impairments; (3) lixisenatide inhibited the Aβ25-35 injection-induced activation of glycogen synthase kinase 3β (GSK3β), with a significant increase in the phosphorylation of ser9 and a significant decrease in the phosphorylation of Y216. These results indicate that lixisenatide, by affecting the PI3K-Akt-GSK3β pathway, can prevent Aβ-related impairments in synaptic plasticity and spatial memory of rats, suggesting that lixisenatide may be a novel and effective treatment for AD.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience - Volume 277, 26 September 2014, Pages 6-13
Journal: Neuroscience - Volume 277, 26 September 2014, Pages 6-13
نویسندگان
H.-Y. Cai, C. Hölscher, X.-H. Yue, S.-X. Zhang, X.-H. Wang, F. Qiao, W. Yang, J.-S. Qi,