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》 2012, 24(3): 297-303
Ca2+失调与阿尔茨海默病发生发展关系的研究进展
林如意,邓天翔,张俊芳,王钦文*
(宁波大学医学院神经科学研究中心,宁波 315211)
文章编号:1004-0374(2012)02-0297-07

摘 要:阿尔茨海默病(Alzheimer’s disease, AD) 是全球老年人中最常见的神经退行性疾病。在对家族性AD 的动物模型和个别AD 患者死后脑组织的研究中发现,除了Aβ42 水平升高外,神经元内Ca2+ 信号失调,并且Ca2+ 信号蛋白表达水平也发生了改变。淀粉样蛋白斑、神经元纤维缠结和神经元丢失是AD的后期标志,它们的共同点可能是破坏神经元钙离子信号。细胞内钙离子水平提高在功能上与淀粉样蛋白斑、早老素突变、tau 缠结和突触功能障碍相关,基于这些研究,产生了AD 的Ca2+ 假说。主要介绍神经元内Ca2+ 失调与AD的关系以及钙拮抗剂作为AD 的潜在治疗方法。
关键词:阿尔茨海默病; Ca2+; β- 淀粉样蛋白; 钙拮抗剂
中图分类号:R749.16; R971.4 文献标志码:A
 
Progress of the relationship between Ca2+ dysregulation and Alzheimer’s disease development
LIN Ru-Yi, DENG Tian-Xiang, ZHANG Jun-Fang, WANG Qin-Wen*
(Behaviour Neuroscience Research Center, School of Medicine, Ningbo University,Ningbo 315211, China)

Abstract: Alzheimer’s disease (AD) is the most common neurodegenerative disorder among the aged in the world. In addition to the increase in Aβ42 levels, disturbances in neuronal calcium(Ca2+) signaling and alterations in expression levels of Ca2+ signaling proteins have been observed in animal models of familial AD and in studies of postmortem brain samples from sporadic AD patients. Although amyloid plaques, neurofibrillary tangles and neuronal loss are late stage markers of AD, one common element of them is disrupted neuronal calcium signaling. Increased intracellular calcium levels are functionally linked to amyloid plaques, presenilin mutations, tau tangles and synaptic dysfunction. Based on these studies, the Ca2+ hypothesis of AD has been proposed. In this review, we discuss the relationship between Ca2+ dysregulation and AD, and Ca2+ blockers may be potential AD treatments.
Key words: Alzheimer’s disease; Ca2+; β-amyloid; calcium antagonists
 
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