کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8271011 | 1534977 | 2013 | 50 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Antisense directed against PS-1 gene decreases brain oxidative markers in aged senescence accelerated mice (SAMP8) and reverses learning and memory impairment: A proteomics study
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کلمات کلیدی
AβSAMAPPPS-2NFTPresenilin-1PS-1BCIP/NBT - BCIP / NBTantisense oligonucleotide - oligonucleotide antisensepresenilin-2 - Presenilin-2Senescence accelerated mouse - Senescence ماوس را تسریع کردamyloid β-peptide - β-پپتید آمیلوئیدmild cognitive impairment - اختلال شناختی خفیفFAD - بدAlzheimer's disease - بیماری آلزایمرfamilial Alzheimer's disease - بیماری آلزایمر خانوادگیMCI - همراه اولamyloid precursor protein - پروتئین پیش ماده آمیلوئی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
سالمندی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
ABSTRACTAmyloid β-peptide (Aβ) plays a central role in the pathophysiology of Alzheimer's disease (AD) through the induction of oxidative stress. This peptide is produced by proteolytic cleavage of amyloid precursor protein (APP) by the action of β- and γ-secretases. Previous studies demonstrated that reduction of Aβ, using an antisense oligonucleotide (AO) directed against the Aβ region of APP, reduced oxidative stress-mediated damage and prevented or reverted cognitive deficits in senescence-accelerated prone mice (SAMP8), a useful animal model for investigating the events related to Aβ pathology and possibly to the early phase of AD. In the current study, aged SAMP8 were treated by AO directed against PS-1, a component of the γ-secretase complex, and tested for learning and memory in T-maze foot shock avoidance and novel object recognition. Brain tissue was collected to identify the decrease of oxidative stress and to evaluate the proteins that are differently expressed and oxidized after the reduction in free radical levels induced by Aβ. We used both expression proteomics and redox proteomics approaches. In brain of AO-treated mice a decrease of oxidative stress markers was found, and the proteins identified by proteomics as expressed differently or nitrated are involved in processes known to be impaired in AD. Our results suggest that the treatment with AO directed against PS-1 in old SAMP8 mice reverses learning and memory deficits and reduces Aβ-mediated oxidative stress with restoration to the normal condition and identifies possible pharmacological targets to combat this devastating dementing disease.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Free Radical Biology and Medicine - Volume 65, December 2013, Pages 1-14
Journal: Free Radical Biology and Medicine - Volume 65, December 2013, Pages 1-14
نویسندگان
Ada Fiorini, Rukhsana Sultana, Sarah Förster, Marzia Perluigi, Giovanna Cenini, Chiara Cini, Jian Cai, Jon B. Klein, Susan A. Farr, Michael L. Niehoff, John E. Morley, Vijaya B. Kumar, D. Allan Butterfield,