中国科技核心期刊
CN:31-1600/Q
ISSN:1004-0374
“健康与疾病的免疫”国际学术研讨会通知      关于有网站冒充本刊网站的声明
《生命科学》 2014, 26(6): 550-559
老年痴呆症的分子机制
沈 阳1,2,3,陈 宇1,2,3,傅洁瑜1,2,3,叶玉如1,2,3*
(1 香港科技大学深圳研究院广东省脑科学及疾病与药物研究重点实验室,深圳 518057;
    2 香港科技大学分子神经科学国家重点实验室,香港;3 香港科技大学生命科学部和分子神经科学中心,香港)
老年痴呆症是一种多发于老年人群的神经退行性疾病,其发病机理十分复杂,目前主要认为与β-淀粉样蛋白的神经毒性和微管结合蛋白tau 的异常修饰相关。将从β- 淀粉样蛋白在神经突触功能失调、神经元凋亡、炎症反应中的作用,以及tau 蛋白异常修饰的机理与神经损伤等方面阐述老年痴呆症发病的分子机理,并对相关诊断和治疗手段进行讨论。
 
Molecular mechanisms underlying the pathophysiology
SHEN Yang1,2,3, CHEN Yu1,2,3, FU Amy Kit-Yu1,2,3, IP Nancy Y1,2,3*
(1 Guangdong Key Laboratory of Brain Science, Disease and Drug Development, HKUST Shenzhen Research Institute, Shenzhen 518057, China; 2 State Key Laboratory of Molecular Neuroscience, The Hong Kong University of Science and Technology, Hong Kong, China; 3 Division of Life Science and Molecular Neuroscience Center, The Hong Kong University of Science and Technology, Hong Kong, China)
Alzheimer’s disease (AD) is one of the most common neurodegenerative diseases in the elderly population. It is believed that β-amyloid-induced toxicity and the abnormal modification of the microtubule binding protein tau are two major pathogenic factors that contribute to AD. In this article, we will discuss the molecular mechanisms underlying AD, including the impaired synaptic transmission, neuronal apoptosis and inflammation induced by β-amyloid, and tau hyperphosphorylation-related neuronal dysfunction. Potential diagnostic and therapeutic approaches will also be discussed.
 
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