Escitalopram attenuates beta-amyloid-induced tau hyperphosphorylation in primary hippocampal neurons through the 5-HT1A receptor mediated Akt/GSK-3 beta pathway

CORC > 昆明动物研究所 > 昆明动物研究所 > 动物模型与人类重大疾病机理重点实验室 > 学习记忆的分子神经机制

	Escitalopram attenuates beta-amyloid-induced tau hyperphosphorylation in primary hippocampal neurons through the 5-HT1A receptor mediated Akt/GSK-3 beta pathway
	Wang YJ 1; Ren QG[]1; Li XL 1; Wu FF 1; Bai F 1; Xu L 2; Zhang ZJ[]1,3; Gong WG 1,2; Wu D 1; Tang X 1
刊名	ONCOTARGET
	2016
卷号	7 期号:12 页码:13328-13339
关键词	Alzheimer's disease tau protein escitalopram Akt/GSK-3 beta pathway 5-HT1A receptor Gerotarget
通讯作者	renqingguo1976@163.com
英文摘要	Tau hyperphosphorylation is an important pathological feature of Alzheimer's disease (AD). To investigate whether escitalopram could inhibit amyloid-beta (A beta)induced tau hyperphosphorylation and the underlying mechanisms, we treated the rat primary hippocampal neurons with A beta(1-42) and examined the effect of escitalopram on tau hyperphosphorylation. Results showed that escitalopram decreased A beta(1-42)-induced tau hyperphosphorylation. In addition, escitalopram activated the Akt/GSK-3 beta pathway, and the PI3K inhibitor LY294002 blocked the attenuation of tau hyperphosphorylation induced by escitalopram. Moreover, the 5-HT1A receptor agonist 8-OH-DPAT also activated the Akt/GSK-3 beta pathway and decreased A beta(1-42)-induced tau hyperphosphorylation. Furthermore, the 5-HT1A receptor antagonist WAY-100635 blocked the activation of Akt/GSK-3 beta pathway and the attenuation of tau hyperphosphorylation induced by escitalopram. Finally, escitalopram improved A beta(1-42) induced impairment of neurite outgrowth and spine density, and reversed A beta(1-42) induced reduction of synaptic proteins. Our results demonstrated that escitalopram attenuated A beta(1-42)-induced tau hyperphosphorylation in primary hippocampal neurons through the 5-HT1A receptor mediated Akt/GSK-3 beta pathway.
收录类别	SCI
资助信息	This work was supported by grants from the National Natural Science Foundation of China (91232707 Qing- guo Ren, 81420108012 Zhi-jun Zhang, 81501173 Xiao-li Li), the National Major Science and Technology Program of China (No. 2012ZX09506-001-009 Zhi-Jun Zhang), the Key Program for Clinical Medicine and Science and Technology, Jiangsu Provincial Clinical Medical Research Center (BL2013025), National High-tech R.D Program (863 Program) (No.2015AA020508), National Basic Research Program of China (2013CB835103) and Strategic Priority Research Program of Chinese Academy of Science (XDB02020002).
内容类型	期刊论文
源URL	[http://159.226.149.26:8080/handle/152453/10312]
专题	昆明动物研究所_学习记忆的分子神经机制昆明动物研究所_动物模型与人类重大疾病机理重点实验室
作者单位	1.Department of Neurology, ZhongDa Hospital, Neuropsychiatric Institute, Medical School of Southeast University, Nanjing, China 2.Key Laboratory of Animal Models and Human Disease Mechanisms, Chinese Academy of Sciences & Yunnan Province, Kunming Institute of Zoology, Kunming, Yunnan, China 3.Center of Schizophrenia, Beijing Institute for Brain Disorders, Beijing, China
推荐引用方式 GB/T 7714	Wang YJ,Ren QG[*],Li XL,et al. Escitalopram attenuates beta-amyloid-induced tau hyperphosphorylation in primary hippocampal neurons through the 5-HT1A receptor mediated Akt/GSK-3 beta pathway[J]. ONCOTARGET,2016,7(12):13328-13339.
APA	Wang YJ.,Ren QG[*].,Li XL.,Wu FF.,Bai F.,...&Tang X.(2016).Escitalopram attenuates beta-amyloid-induced tau hyperphosphorylation in primary hippocampal neurons through the 5-HT1A receptor mediated Akt/GSK-3 beta pathway.ONCOTARGET,7(12),13328-13339.
MLA	Wang YJ,et al."Escitalopram attenuates beta-amyloid-induced tau hyperphosphorylation in primary hippocampal neurons through the 5-HT1A receptor mediated Akt/GSK-3 beta pathway".ONCOTARGET 7.12(2016):13328-13339.