【摘要】 目的:探讨携带5个家族性基因突变的APP/PS1转基因阿尔茨海默病(AD)(5×FAD)模型小鼠海马CA1区神经元突触超微结构改变。方法:应用透射电镜观察和形态计量学分析5×FAD转基因AD鼠海马CA1区GrayⅠ型突触界面结构参数,包括突触间隙长度、突触间隙面积、突触后致密物浓度和突触界面曲率的变化。结果:5×FAD转基因AD鼠海马CA1区神经元突触活性区长度显著小于对照组,差异有统计学意义;突触后致密物厚度、突触界面曲率及宽度与对照组差异无统计学意义。结论:5个家族性突变基因导致小鼠海马CA1区神经元突触可塑性的改变,这可能是该突变基因导致的发病机制之一。更多还原

【Abstract】 Objective: To analyze ultrastructure changes of neuronal synapse in area CAl of the hippocampus of five familiar APP/PS1 tramsgenic mouse with Alzheimer’s disease(5×FAD). Methods: The length of synaptic cleft, area of synaptic cleft, thickness of postsynaptic density, and curvature of synapse active zone were measured in the interface of synapse by morphometry analysis. Results : The length of synaptic cleft in 5 X FAD mice group was significantly shorter than that in control group. There were no significant differences between 5 × FAD mice group and control group in the area of synaptic cleft, thickness of postsynaptic density and curvature of synapse active zone. Conclusion: The gene of 5×FAD can induce the change of synaptic plasticity in area CA1 of the hippocampus, which may be one of the mechanisms for these genes to induce Alzheimer’s disease.更多还原