脂肪因子参与阿尔茨海默病的研究进展  

Progress on Adipokines Participating in Alzheimer's Disease

作　　者：罗飘[1,2] 楚世峰 陈乃宏 LUO Piao;CHU Shi-feng;CHEN Nai-hong(College of Pharmacy,Hunan University of Chinese Medcine,410208,China;Neuroscience Center,Institute of Materia Medica,Chinese Academy of Medical Sciences and Peking Union Medical College,Beijing,100050,China)

机构地区：[1]湖南中医药大学药学院,长沙410208 [2]中国医学科学院,药物研究所&神经科学中心,北京100050

出　　处：《神经药理学报》2017年第1期45-52,共8页Acta Neuropharmacologica

基　　金：国家自然科学基金项目(No.81274122、81373997、81273629、21272278、U1402221、81260650);北京市自然科学基金项目(No.7131013、7142115);湖南省重点研发计划项目(No.2015SK2029-1);湖南省教育厅高校科研经费开放基金项目(No.15K091);新药作用机制研究与药效评价北京市重点实验室资助项目(No.BZ0150)

摘　　要：阿尔茨海默病(Alzheimer’s disease,AD)又称老年痴呆,是一种最常见的老年中枢神经退行性疾病。其主要病理改变有:神经元外β-淀粉样蛋白(β-amyloid protein,Aβ)沉积形成的老年斑、神经元内tau蛋白异常磷酸化形成的神经原纤维缠结以及神经元大量丢失或损伤。近年研究发现,脂肪因子与Aβ沉积、tau蛋白过度磷酸化以及神经元凋亡之间具有紧密的联系。该文主要针对脂联素(adiponectin,APN)、瘦素(leptin,LP)、白细胞介素-6(interleukin-6,IL-6)等脂肪因子对AD的作用机制做一综述,为AD的临床治疗提供新的思路。Alzheimer's disease(AD),also called senile dementia,is one of the most common central neurodegenerative disease in the elderly.And its main pathological changes include the senile plaques formed byβ-amyloid protein deposition out of the neuron,neurofibrillary tangles caused by the hyperphosphorylated tau protein in the neuron,and neurons in large number of loss and damage.Recently,the study has showed that Adipokine has closed relationship betweenβ-amyloid protein deposition,hyperphosphorylated tau protein and neuronal apoptosis.This paper is mainly about the effect and mechanism of Adipokine,such as adiponectin,leptin,interleukin-6and so on,on AD,which aims to provide a new ideas for the clinical treatment of AD.

关 键 词：阿尔茨海默病 脂肪因子 脂联素 瘦素 白细胞介素-6 

分 类 号：R964[医药卫生—药理学]