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Ribosylation-Derived Advanced Glycation End Products Induce Tau Hyperphosphorylation Through Brain-Derived Neurotrophic Factor Reduction

文献类型：期刊论文

作者Wu, Beibei1; Wang, Yujing1; Shi, Chenggang1; Chen, Yao2; Yu, Lexiang1; Li, Juan3; Li, Weiwei5; Wei, Yan1; He, Rongqiao1,4
刊名JOURNAL OF ALZHEIMERS DISEASE
出版日期2019
卷号71期号:1页码:291-305
ISSN号1387-2877
关键词Advanced glycation end products brain-derived neurotrophic factor GSK-3 beta oxidative stress ribosylation tau hyperphosphorylation
DOI10.3233/JAD-190158
通讯作者Wei, Yan(yanwei@ibp.ac.cn) ; He, Rongqiao(herq@ibp.ac.cn)
英文摘要Advanced glycation end products (AGEs) have been implicated in the disease process of diabetes mellitus. They have also been found in senile plaques and neurofibrillary tangles in the brains of Alzheimer's disease patients. Furthermore, abnormally high levels of D-ribose and D-glucose were found in the urine of patients with type 2 diabetes mellitus, suggesting that diabetic patients suffer from dysmetabolism of not only D-glucose but also D-ribose. In the present study, intravenous tail injections of ribosylated rat serum albumin (RRSA) were found to impair memory in rats, but they did not markedly impair learning, as measured by the Morris water maze test. Injections of RRSA were found to trigger tau hyperphosphorylation in the rat hippocampus via GSK-3 beta activation. Tau hyperphosphorylation and GSK-3 beta activation were also observed in N2a cells in the presence of ribosylation-derived AGEs. Furthermore, the administration of ribosylation-derived AGEs induced the suppression of brain-derived neurotrophic factor (BDNF) and tropomyosin-related kinase B (TrkB). Both GSK-3 beta inhibition and BDNF treatment decreased the levels of phosphorylated tau in N2a cells. In particular, the administration of BDNF could rescue memory failure in ribosylated AGE-injected rats. Ribosylation-derived AGEs downregulated the BDNF-TrkB pathway in rat brains and N2a cells, leading to GSK-3 beta activation-mediated tau hyperphosphorylation, which was involved in the observed rat memory loss. Targeting ribosylation may be a promising therapeutic strategy to prevent Alzheimer's disease and diabetic encephalopathies.
WOS关键词GROWTH-FACTOR EXPRESSION ; D-RIBOSE ; ALZHEIMERS-DISEASE ; PROTEIN ; MEMORY ; BDNF ; TERM ; HIPPOCAMPUS ; MECHANISM ; STRESS
资助项目National Key Research and Development Program of China[2016YFC1305900] ; National Key Research and Development Program of China[2016YFC1306300] ; Beijing Municipal Science and Technology Project[Z161100000217141] ; Beijing Municipal Science and Technology Project[Z161100000216137] ; Natural Scientific Foundation of China NSFC[31670805] ; Natural Scientific Foundation of China NSFC[81573763] ; Youth Innovation Promotion Association CAS[2017132] ; 973 Project[2012CB911004] ; External Cooperation Program of BIC, Chinese Academy of Sciences[GJHZ201302]
WOS研究方向Neurosciences & Neurology
语种英语
出版者IOS PRESS
WOS记录号WOS:000484216500023
资助机构National Key Research and Development Program of China ; Beijing Municipal Science and Technology Project ; Natural Scientific Foundation of China NSFC ; Youth Innovation Promotion Association CAS ; 973 Project ; External Cooperation Program of BIC, Chinese Academy of Sciences
源URL[http://ir.psych.ac.cn/handle/311026/29837]  
专题心理研究所_脑与认知科学国家重点实验室
通讯作者Wei, Yan; He, Rongqiao
作者单位1.Univ Chinese Acad Sci, Inst Biophys, State Key Lab Brain & Cognit Sci, Beijing, Peoples R China
2.Southwest Med Univ, Luzhou, Sichuan, Peoples R China
3.Chinese Acad Sci, Inst Psychol, Key Laboratoty Mental Hlth, Beijing, Peoples R China
4.Capital Med Univ, Alzheimers Dis Ctr, Beijing Inst Brain Disorders, Beijing, Peoples R China
5.Peking Univ Hosp, Beijing, Peoples R China
推荐引用方式
GB/T 7714		 Wu, Beibei,Wang, Yujing,Shi, Chenggang,et al. Ribosylation-Derived Advanced Glycation End Products Induce Tau Hyperphosphorylation Through Brain-Derived Neurotrophic Factor Reduction[J]. JOURNAL OF ALZHEIMERS DISEASE,2019,71(1):291-305.
APA Wu, Beibei.,Wang, Yujing.,Shi, Chenggang.,Chen, Yao.,Yu, Lexiang.,...&He, Rongqiao.(2019).Ribosylation-Derived Advanced Glycation End Products Induce Tau Hyperphosphorylation Through Brain-Derived Neurotrophic Factor Reduction.JOURNAL OF ALZHEIMERS DISEASE,71(1),291-305.
MLA Wu, Beibei,et al."Ribosylation-Derived Advanced Glycation End Products Induce Tau Hyperphosphorylation Through Brain-Derived Neurotrophic Factor Reduction".JOURNAL OF ALZHEIMERS DISEASE 71.1(2019):291-305.

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来源：心理研究所

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