首页> 美国卫生研究院文献>Journal of Visualized Experiments : JoVE >Establishment of a Valuable Mimic of Alzheimers Disease in Rat Animal Model by Intracerebroventricular Injection of Composited Amyloid Beta Protein
【2h】

Establishment of a Valuable Mimic of Alzheimers Disease in Rat Animal Model by Intracerebroventricular Injection of Composited Amyloid Beta Protein

机译:大鼠脑室内注射复合淀粉样β蛋白在大鼠动物模型中建立重要的阿尔茨海默氏病模拟物

代理获取
本网站仅为用户提供外文OA文献查询和代理获取服务,本网站没有原文。下单后我们将采用程序或人工为您竭诚获取高质量的原文,但由于OA文献来源多样且变更频繁,仍可能出现获取不到、文献不完整或与标题不符等情况,如果获取不到我们将提供退款服务。请知悉。

摘要

Alzheimer's disease (AD) is an irreversible, progressive brain disease that slowly destroys memory and is accompanied by neuron loss and structure change. With the increase of AD patients worldwide, the pathology and treatment of the disease has become a focus in the International Pharmaceutical Industry. Thus, the establishment of the animal model to mimic AD in the laboratory is of great importance.Here, we describe a detailed protocol for establishing a mimic of AD in a rat animal model though intracerebroventricular injection of amyloid beta protein 25-35 (Aβ25-35) combined with aluminum trichloride (AlCl3) and anterodorsal thalamic nucleus injection of recombinant human transforming growth factor-β1 (RHTGF-β1) to rats. The related markers of AD were measured, including: spatial memory, neuronal structure and substructure, neuronal Aβ, and neurofibrillary tangles (NFT) production. This rat model demonstrates spatial memory impairment, neuronal structure and substructure pathological changes, neuron intracellular Aβ burden, and NFT aggregation, and provides a close mimic of the neuronal structure and function disorder to that of clinical AD patients. Thus, the presented AD rat modelprovides a valuable in vivo tool for exploring neuronal function, neuronal pathology, and drug screening of AD.
机译:阿尔茨海默氏病(AD)是一种不可逆的进行性脑部疾病,会慢慢破坏记忆力,并伴有神经元丢失和结构改变。随着全世界AD患者的增加,该疾病的病理学和治疗已成为国际制药工业的关注焦点。因此,在实验室中建立模拟AD的动物模型非常重要。在这里,我们描述了通过脑室内注射淀粉样β蛋白25-35(Aβ25- 35)结合三氯化铝(AlCl3)和丘脑前丘脑核向大鼠注射重组人转化生长因子-β1(RHTGF-β1)。测量了AD的相关标志,包括:空间记忆,神经元结构和亚结构,神经元Aβ和神经原纤维缠结(NFT)产生。该大鼠模型证明了空间记忆障碍,神经元结构和亚结构的病理变化,神经元细胞内Aβ负担和NFT聚集,并且提供了与临床AD患者相似的神经元结构和功能障碍的模拟方法。因此,提出的AD大鼠模型为探索AD的神经元功能,神经病理学和药物筛选提供了一种有价值的体内工具。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
代理获取

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号