STUDY ON BIOCHEMICAL CHARACTERIZATION OF SENILE NEURONAL CYTOSKELETAL ABBERATION
老年神经元细胞骨架畸变的生化特征研究
基本信息
- 批准号:62570488
- 负责人:
- 金额:$ 1.15万
- 依托单位:
- 依托单位国家:日本
- 项目类别:Grant-in-Aid for General Scientific Research (C)
- 财政年份:1987
- 资助国家:日本
- 起止时间:1987 至 1988
- 项目状态:已结题
- 来源:
- 关键词:
项目摘要
Under the purpose of establishing an animal model of cerebrovascular dementia. the bilateral carotid artery of Mongolian gerbil is stenosed with a newly designed clip. showing decreased regional cerebral blood flow to 75 % of the original level for 8 weeks. dysfunction in learning by passive avoidance test. a little morphological evidence of neuronal death in hippocampal caI region. and decreased amount of microtubule-associated protein (HAP) 2.As a neurochemical model of Alzheiemr's diease. rabbits are injected with aluminium salt. resulting in formation of experimental neurofibrillary change. The rabbit brain with experimental neurofibrillary change is studied and the activity of seven lysosomal enzymes is assaged. showing increased activity of cathepsin D enzyme. The cathepsin D enzyme from the aluminium injected rabbit brain is purified by affinity chromatography. The molecular and emzymological characterization of the pathological cathepsin D shows the same molecular weight. same amino acid composition. but different Km and Vmax values, and different pattern of heat denaturation. Further, the instability of the lysosome membrame is demonstrated in the aged rat brain, which could partially explain the increased activity of cathepsin D in model animal of Alzheimer's disease.Under the purpose of finding a biological marker of Alzheimer's disease. the serum autoantibody titer to glial fibrillary acidic protein (GFAP) is assayed, showing significantly increased antibody titer to GFAP in Alzheimer's disease patient sera but not in that of the healthy control subjects.
目的是建立脑血管性痴呆动物模型。用一种新设计的夹闭器使长爪沙鼠双侧颈动脉狭窄。显示局部脑血流量降低至原始水平的75%,持续8周。被动回避试验显示学习功能障碍。海马CAI区神经元死亡的形态学证据。微管相关蛋白(HAP)含量降低。2.作为阿尔茨海默病的神经化学模型。给兔子注射铝盐。导致实验性神经病理改变的形成。本文对实验性神经病理改变的兔脑进行了研究,并对七种溶酶体酶的活性进行了测定。显示组织蛋白酶D酶的活性增加。用亲和层析法从注射铝的兔脑中纯化组织蛋白酶D。病理组织蛋白酶D的分子和酶学特征显示相同的分子量。相同的氨基酸组成。但Km和Vmax值不同,热变性方式也不同。此外,老年大鼠脑内溶酶体膜的不稳定性,可部分解释阿尔茨海默病模型动物中组织蛋白酶D活性增高的现象,旨在寻找阿尔茨海默病的生物学标志物。测定了抗胶质细胞酸性蛋白(GFAP)的血清自身抗体滴度,显示在阿尔茨海默病患者血清中抗GFAP的抗体滴度显著增加,但在健康对照受试者中没有。
项目成果
期刊论文数量(24)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
武田雅俊: "細胞骨格の異常アルツハイマー型老年痴呆(最近の知識)" 藤田企画出版, 14 (1988)
武田正敏:“阿尔茨海默病型老年痴呆症的细胞骨架异常(最新知识)”藤田机画出版社,14(1988)
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HIDEO SUZUKI: "NEUROFILAMENT DEGRADATION BY BOVAINE BRAIN CATHEPSIN D" Neurosci.Lett.89. 240-245 (1988)
HIDEO SUZUKI:“牛脑组织蛋白酶 D 导致的神经丝降解”Neurosci.Lett.89。
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- 影响因子:0
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NISHIMURA Tsuyoshi其他文献
NISHIMURA Tsuyoshi的其他文献
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Study about Causes of Alzheimer disease
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03454288 - 财政年份:1991
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$ 1.15万 - 项目类别:
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