کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
6803576 | 1433545 | 2016 | 45 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Ketones block amyloid entry and improve cognition in an Alzheimer's model
ترجمه فارسی عنوان
کتون ها از ورود آمیلوئید جلوگیری می کنند و باعث بهبود شناخت در مدل آلزایمر می شوند
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
سالمندی
چکیده انگلیسی
Sporadic Alzheimer's disease (AD) is responsible for 60%-80% of dementia cases, and the most opportune time for preventive intervention is in the earliest stage of its preclinical phase. As traditional mitochondrial energy substrates, ketone bodies (ketones, for short), beta-hydroxybutyrate, and acetoacetate, have been reported to provide symptomatic improvement and disease-modifying activity in epilepsy and neurodegenerative disorders. Recently, ketones are thought as more than just metabolites and also as endogenous factors protecting against AD. In this study, we discovered a novel neuroprotective mechanism of ketones in which they blocked amyloid-β 42, a pathologic hallmark protein of AD, entry into neurons. The suppression of intracellular amyloid-β 42 accumulation rescued mitochondrial complex I activity, reduced oxidative stress, and improved synaptic plasticity. Most importantly, we show that peripheral administration of ketones significantly reduced amyloid burden and greatly improved learning and memory ability in a symptomatic mouse model of AD. These observations provide us insights to understand and to establish a novel therapeutic use of ketones in AD prevention.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neurobiology of Aging - Volume 39, March 2016, Pages 25-37
Journal: Neurobiology of Aging - Volume 39, March 2016, Pages 25-37
نویسندگان
Jun Xiang Yin, Marwan Maalouf, Pengcheng Han, Minglei Zhao, Ming Gao, Turner Dharshaun, Christopher Ryan, Julian Whitelegge, Jie Wu, David Eisenberg, Eric M. Reiman, Felix E. Schweizer, Jiong Shi,