【摘要】 目的探讨APP/PS1阿尔茨海默病转基因动物模型胼胝体病理学改变。方法取胼胝体作为白质代表区域,采用氯化金髓鞘染色和轴突免疫组织化学染色方法,利用光密度方法对胼胝体轴突密度和髓鞘化程度的染色进行ROD定量分析。结果年龄相关性分析表明,老年组小鼠(包括APP/PS1和PS1)的轴突密度较年轻组小鼠显著下降,然而老年组小鼠的髓鞘化程度较年轻组有所增高。不同表型分析显示,年轻组APP/PS1小鼠的轴突密度和髓鞘化程度和年轻组PS1小鼠一致,然而老年组APP/PS1小鼠轴突密度和髓鞘化程度较老年组PS1小鼠显著下降。结论在APP/PS1阿尔茨海默病转基因动物模型中胼胝体存在着轴突的丢失和脱髓鞘改变,与β淀粉样蛋白对白质的毒性作用有关。更多还原

【Abstract】 Objective To investgate pathological changes in the white matter in APP/PS1 mice modeling Alzheimer’s disease.Methods Myelin was stained with gold chloride and axon was stained with anti-neurofilament M antibody.We took corpus callosum as representative region of white matter and quantitatively analyzed the ROD value of staining with densitometry.Results In the corpus callosum,with aging,a severe decrease in neurofilament staining was observed,both in aged APPxPS1 and PS1 mice;on the other side,an increase of the myelination of the corpus callosum was observed when comparing 2-months and 24-months old PS1 mice.Different phenotype analysis demonstrate that axon density and myelination is comparative in the young APP/PS1 mice and young PS1 mice;while axon density and myelination of aged APP/PS1 mice decreased remarkably than that of aged PS1 control mice.Conclusion There was axon loss and demyelination in the corpus callosum of aged APP/PS1 transgenic Alzheimer’s disease model,and amyloid beta damaged white matter.更多还原