阿尔采末病非人灵长类动物模型  

Progress in the primate models of Alzheimers disease

作　　者：郑元元[1] 孙兰[1] 

机构地区：[1]中国医学科学院.中国协和医科大学基础医学院药理室,北京100005

出　　处：《中国药理学通报》2005年第6期649-653,共5页Chinese Pharmacological Bulletin

摘　　要：阿尔采末病(AD)是一种以进行性认知障碍和记忆力损害为主的中枢神经系统退行性疾病。非人灵长类动物(nonhumanprimate,NHP)模型较啮齿类动物模型更好地模拟了AD的病理变化,其神经生物学特性与人类非常相似,是研究AD等疾病最理想的动物模型,对筛选治疗老年痴呆药也起着至关重要的作用。恒河猴是目前应用最广泛的非人灵长类实验动物,另外松鼠猴、小猿、短尾猿、猩猩、黑猩猩和狐猴也是AD研究的理想实验动物。本文通过非人灵长类动物模型的胆碱能系统、β淀粉样肽沉积、载脂蛋白E、神经元纤维缠结和tau蛋白等方面的变化,对近年来NHP的自发性、诱发性及自身免疫性痴呆模型的发展分别进行阐述。Alzheimers disease (AD) is a progressively and retrogressively neurodegenerative disorder of central nervous system severely threatening the aged. The studies of animal models, which share the very similar neuropathological characteristics with human, provide tools for the understanding of the etiology, mechanisms and medicine screening of AD. The distribution and chemical composition of amyloid-beta (A- beta) peptide -positive deposits were investigated in various non-human primate models. Various proportions of A- beta deposits contained cholinesterase activities, apolipoprotein E(ApoE) and alpha1-antichymotrypsin immunoreactivity. Alterations in the basal forebrain cholinergic system have been widely studied, but the magnitude of decline and relationship to cognitive impairment are still a matter of debate. This article also includes the latest research of the changing on tau, subtle structural alterations in axons, and neurofibrillary tangles (NFT) in the brain tissues of the non-human primate models.

关 键 词：阿尔采末病 老年痴呆 灵长类动物模型 

分 类 号：R-05[医药卫生] R-332