期刊文献+

Comparative study of histopathology changes between the PS1/APP double transgenic mouse model and Aβ_(1-40)-injected rat model of Alzheimer disease 被引量:7

Comparative study of histopathology changes between the PS1/APP double transgenic mouse model and Aβ_(1-40)-injected rat model of Alzheimer disease
下载PDF
导出
摘要 Objective To identify the genetype of the PS1/APP double transgenie mouse model, then to analyse the histopathological changes in the brain and compare the differences between the transgenie mice models and Aβ1-40-injeeted rats models of Alzheimer disease. Methods The modified congo red staining, Nissl's staining and immunohistology staining was used to observe the Aβ deposits, activation of astrocyte respectively. Results ①The PS1/APP transgenic mouse extensively displayed Aβ deposits in the cortex and hippocampal structures, and GFAP positive cells were aggregated in mass and surrounded the congo red-positive plaque. ②The Aβ1-40-intrahippocmnpal-injeeted rat model showed the Aβ plaque deposits in the dentate gyrus of the hippocampus, with the astrocyte surrounded. The neurons loss was significant in the injection point and pin hole of injection with Nissl's staining methods. GFAP-positive cells increased significantly compared with the uninjected lateral of the hippocampus. Conclusion Although Aβ1-40-injected rat models could simulate some characteristic pathological features of human Alzheimer diseases, Aβ deposits and neurons loss in partial hippocampal, it would not simulate the progressive degenenration in the brain of AD. The double transgenie PS1/APP mice could simulate the specific pathogenesis and progressive changes of AD, mainly is Aβ deposits and the spongiocyte response , while no neurons loss were observed in this model. Objective To identify the genetype of the PS1/APP double transgenic mouse model, then to analyse the histopathological changes in the brain and compare the differences between the transgenic mice models and Aβ_(1-40)-injected rats models of Alzheimer disease. Methods The modified congo red staining, Nissl's staining and immunohistology staining was used to observe the Aβ deposits, activation of astrocyte respectively. Results ①The PS1/APP transgenic mouse extensively displayed Aβ deposits in the cortex and hippocampal structures, and GFAP positive cells were aggregated in mass and surrounded the congo red-positive plaque. ②The Aβ_(1-40)-intrahippocampal-injected rat model showed the Aβ plaque deposits in the dentate gyrus of the hippocampus, with the astrocyte surrounded. The neurons loss was significant in the injection point and pin hole of injection with Nissl's staining methods. GFAP-positive cells increased significantly compared with the uninjected lateral of the hippocampus. Conclusion Although Aβ_(1-40)-injected rat models could simulate some characteristic pathological features of human Alzheimer diseases, Aβ deposits and neurons loss in partial hippocampal, it would not simulate the progressive degenenration in the brain of AD. The double transgenie PS1/APP mice could simulate the specific pathogenesis and progressive changes of AD, mainly is Aβ deposits and the spongiocyte response, while no neurons loss were observed in this model.
出处 《Neuroscience Bulletin》 SCIE CAS CSCD 2006年第1期52-57,共6页 神经科学通报(英文版)
基金 This project was supported by the National Natural Science Foundation of China ( No. 30100087, 30500148, 30571770) funded by the Collaborating Research Fund for Young Scholars from Abroad of National Natural Science Foundation of China ( No. 30228018 ).
关键词 Alzheimer disease transgenic mouse RAT Β-AMYLOID 组织病理学说 老年性痴呆 动物实验 小鼠
  • 相关文献

参考文献9

  • 1Selkoe DJ. Alzheimer' s disease: genes, proteins, and therapy.Physiol Rev, 2001,81 (2):741-766.
  • 2Hardy J. The amyloid hypothesis of Alzheimer' s disease: progress and problems on the road to the therapeutics Science,2002,297:353 -356.
  • 3Forloni G,Tagliavini F,Bugiani O, et al. Amyloid in Alzheimer's disease and prion-related encephalopathies: studies with synthetic peptides. Prog Neurobiol, 1996, 49:287-315.
  • 4Oddo S, Caccamo A, LaFerla FM, et al. Triple-Tranagenic Model of Alzheimer' s disease with plaques and tangles: intracellular aβand synaptic dysfunction. Neuron, 2003,39:409-421.
  • 5Price DL, Tanzi RE, Borchelt DR, et al. Sisodia Alzheimer' s disease: genetic studies and transgenic models. Annu Roy Genet,1998, 32 : 461-493.
  • 6Leuven FV. Single and multiple transgenic mice as models for Alzheimer's disease. Prog Neurobiol, 2000, 61 (3) :305-312.
  • 7Borchelt DR, Ratoviski T, Lare J, et al. Accelerated amyloid deposition in the brains of transgenic mice coexpressing mutant presenilin 1 and amyloid precursor proteins. Neuron, 1997, 19 (4) :939-945.
  • 8James C, Hittner JM, Semotuk M, et al. Beta-amyloid(1-40)effects on behavior and memory. Brain Res, 1995, 682: 69-74.
  • 9Combs C K, Johnson DE, Cannady SB,et al. Identification of microglial signal traneduction pathways mediating a neurotoxic response to amyloidogenic fragments of beta-amyloid and prion proteins. J Neurosci, 1999,19 : 928-939.

同被引文献12

引证文献7

二级引证文献29

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部