【摘要】 目的探究阿尔茨海默病(AD)模型小鼠(APPswe/PS1dE9双转基因小鼠)中出现的神经元轴突异常及其可能的发生机制。方法 RT-qPCR分别测定野生型及APPswe/PS1dE9双转基因小鼠体内神经突起导向因子(netrin)和结肠癌缺失基因(DCC)的表达量;用免疫细胞染色分别测量其海马区神经元轴突长度。结果与野生型相比,APPswe/PS1dE9双转基因小鼠海马区神经元轴突出现明显的缩短,且其脑内netrin-1(P<0. 001)、DCC1和DCC2的表达量均有上升(P<0. 01)。结论轴突的变化与AD的发生存在一定联系,这样的联系可能通过netrin-1与DCC的相互作用产生。更多还原

【Abstract】 Objective To study the axon abnormalities and possible underlying mechanisms in APPswe/PS1 dE9 double-transgenic mice,as the model of Alzheimer’s disease( AD). Methods With RT-qPCR,the expression of netrin( netrin-1 and netrin-3) and DCC( DCC1 and DCC2) was determined in wild type mice and APPswe/PS1 dE9 double-transgenic mice separately,while the changes of axon length in hippocampus neurons were calculated using immunocytofluorescence. Results Compared with wild type mice, the expression of netrin-1( P < 0. 001),DCC1 and DCC2( P < 0. 01) were all up regulated in APPswe/PS1 dE9 double-transgenic mice. At the same time,the double transgenic mice showed decrease in axon length in hippocampus neurons. Conclusions Abnormalities in axon are found in connection with AD,and interactions in netrin-1 and DCC can be responsible for this relationship.更多还原