کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8281040 | 1535145 | 2012 | 5 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Advanced glycation end products and neurodegenerative diseases: Mechanisms and perspective
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
سالمندی
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چکیده انگلیسی
The age-related neurodegenerative disorders such as Alzheimer's, Parkinson's, and Huntington's diseases are characterized by the abnormal accumulation or aggregation of proteins. Advanced glycation end products (AGEs) are proteins or lipids that become glycated after exposure to sugars. The formation of AGEs promotes the deposition of proteins due to the protease resistant crosslinking between the peptides and proteins. Several proteins implicated in neurodegenerative diseases such as amyloid β, tau, α-synuclein, and prions are glycated and the extent of glycation is correlated with the pathologies of the patients. These data suggest that AGEs contribute to the development of neurodegenerative diseases. In this review we summarize recent advances on the investigation of the roles of AGEs in neurodegenerative diseases, with special focus on Alzheimer's and Parkinson's diseases. It is clear that AGEs modification triggers the abnormal deposition and accumulation of the modified proteins, which in turn sustain the local oxidative stress and inflammatory response, eventually leading to the pathological and clinical aspects of neurodegenerative diseases. Further characterization of the molecular mechanisms responsible for AGEs mediated neurotoxicity will provide important clues on the development of novel strategies for the prevention and treatment of neurodegenerative diseases.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Journal of the Neurological Sciences - Volume 317, Issues 1â2, 15 June 2012, Pages 1-5
Journal: Journal of the Neurological Sciences - Volume 317, Issues 1â2, 15 June 2012, Pages 1-5
نویسندگان
Jinlong Li, Danian Liu, Ling Sun, Yunting Lu, Zhongling Zhang,