Scheff Stephen W, Price Douglas A
Sanders-Brown Center on Aging, University of Kentucky College of Medicine, 800 S. Limestone, Lexington, KY 40536-0230, USA.
Neurobiol Aging. 2003 Dec;24(8):1029-46. doi: 10.1016/j.neurobiolaging.2003.08.002.
Morphologic studies of the neuropathology in Alzheimer's disease (AD) have demonstrated significant loss of synaptic connectivity in many regions of the neocortex and hippocampus. The strongest correlation with cognitive decline in AD is with the synaptic density. This article discusses the ultrastructural studies that have documented changes in synaptic numbers in many areas of association cortex and in the hippocampal dentate gyrus molecular layer. Changes in the synaptic complex are discussed as a possible compensatory mechanism in response to synapse loss and a model is proposed to help relate the significance of these synaptic changes. Comparisons are made between results observed with ultrastructural technique and those utilizing immunohistochemistry to assess changes in synaptic pathology. Possible reasons underlying the synaptic neuropathology are discussed.
阿尔茨海默病(AD)神经病理学的形态学研究表明,新皮层和海马体的许多区域存在明显的突触连接丧失。AD中与认知衰退最强的关联是与突触密度相关。本文讨论了超微结构研究,这些研究记录了联合皮层的许多区域以及海马齿状回分子层中突触数量的变化。讨论了突触复合体的变化作为对突触丧失的一种可能的补偿机制,并提出了一个模型来帮助关联这些突触变化的意义。对超微结构技术观察到的结果与利用免疫组织化学评估突触病理学变化的结果进行了比较。还讨论了突触神经病理学背后的可能原因。