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Alzheimer病动物模型的构建及其分子病理学的变化 被引量:2

Study on the construction of animal model for Alzheimer's disease and its change of molecular pathology
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摘要 目的建立能够在行为、生物化学以及组织病理方面较好地模拟AD的动物模型。方法采用MR I,γ-刀立体定位射频热凝损毁老年猴脑的穹隆-海马伞建立动物模型;应用Hedreen方法、免疫组织化学ABC法检测AD动物模型的分子病理学的变化。结果损伤侧海马CA1区的AchE阳性纤维密度明显低于对侧未损伤的对应区的纤维密度;动物模型大脑皮质的大锥体神经元胞体中均可见APPA4的免疫活性物质、抗Tau免疫活性物质沉着,形态上有的近似人AD的老年斑;大脑损伤侧内侧隔核的ChAT阳性神经元的数目明显少于对侧。结论所建立的AD动物模型在理论和实验中接近于AD的病理改变。 Objective To construct a mammal model simulating Alzheimer's disease (AD) from the aspects of behavior,biochemistry and histopathology. Methods The fornix-hippocampal fimbria in aged monkeys was impaired by stereotaxic radio therapeutic ( γ-knife ) radiofrequency thermocoagulation lesion (RFTL) with magnetic resonance imaging (MRI) to establish the animal model and determine its molecular pathological change with Hedreen's method and immunohistochemistry ABC method. Results The neurofiber density of positive acethylcholinesterase (AchE) in impaired hoppocampal CA1 was lower than that in the corresponding of unimpaired side. The immunocompetence substances of APPA4 and anti-Tau similar to human senile plaque were found in hippocampal pyramidal neurons of animal model. Choline acetyltransferas (CHAT) positive neurons in impaired side were lower than those in unimpaired side. Conclusions The established AD animal model could approach to pathological changes of AD from theory and experiments.
出处 《中国老年学杂志》 CAS CSCD 北大核心 2005年第9期1069-1071,共3页 Chinese Journal of Gerontology
基金 国家高技术研究发展计划"863"基金资助项目(编号2001AA217161)
关键词 老年性痴呆 恒河猴 神经纤维缠结 老年斑 TAU蛋白 乙酰胆碱酯酶 胆碱乙酰转移酶 Alzheimer disease (AD) Rhesus Neurofibrillary tangles Senile plaque Microtubule associated protein Tau Acethylcholinesterase (AchE) Choline acetyltransferas (CHAT)
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