Brendza Robert P, O'Brien Cara, Simmons Kelly, McKeel Daniel W, Bales Kelly R, Paul Steven M, Olney John W, Sanes Joshua R, Holtzman David M
Center for the Study of Nervous System Injury, Washington University School of Medicine, St. Louis, Missouri 63110, USA.
J Comp Neurol. 2003 Feb 17;456(4):375-83. doi: 10.1002/cne.10536.
Neuritic plaques are one of the stereotypical hallmarks of Alzheimer's disease (AD) pathology. These structures are composed of extracellular accumulations of fibrillar forms of the amyloid-beta peptide (Abeta), a variety of other plaque-associated proteins, activated glial cells, and degenerating nerve processes. To study the neuritic toxicity of different structural forms of Abeta in the context of regional connectivity and the entire cell, we crossed PDAPP transgenic (Tg) mice, a model with AD-like pathology, to Tg mice that stably express yellow fluorescent protein (YFP) in a subset of neurons in the brain. In PDAPP; YFP double Tg mice, markedly enlarged YFP-labeled axonal and dendritic varicosities were associated with fibrillar Abeta deposits. These varicosities were absent in areas where there were nonfibrillar Abeta deposits. Interestingly, YFP-labeled varicosities revealed changes that corresponded with changes seen with electron microscopy and the de Olmos silver staining technique. Other silver staining methods and immunohistochemical localization of phosphorylated neurofilaments or phosphorylated tau were unable to detect the majority of these dystrophic neurites. Some but not all synaptic vesicle markers accumulated abnormally in YFP-labeled varicosities associated with neuritic plaques. In addition to the characterization of the effects of Abeta on axonal and dendritic structure, YFP-labeled neurons in Tg mice should prove to be a valuable tool to interpret the localization patterns of other markers and for future studies examining the dynamics of axons and dendrites in a variety of disease conditions in living tissue both in vitro and in vivo.
神经炎性斑块是阿尔茨海默病(AD)病理典型的标志性特征之一。这些结构由细胞外淀粉样β肽(Aβ)的纤维状形式、多种其他与斑块相关的蛋白质、活化的胶质细胞以及退化的神经突起聚集物组成。为了在区域连接性和整个细胞的背景下研究不同结构形式的Aβ的神经毒性,我们将具有AD样病理的模型——PDAPP转基因(Tg)小鼠与在大脑中一部分神经元中稳定表达黄色荧光蛋白(YFP)的Tg小鼠进行杂交。在PDAPP;YFP双转基因小鼠中,明显增大的YFP标记的轴突和树突膨体与纤维状Aβ沉积物相关。在存在非纤维状Aβ沉积物的区域中不存在这些膨体。有趣的是,YFP标记的膨体显示出的变化与电子显微镜和德奥尔莫斯银染色技术所观察到的变化相对应。其他银染色方法以及磷酸化神经丝或磷酸化tau的免疫组织化学定位无法检测到这些营养不良性神经突中的大多数。一些但并非所有的突触小泡标记物在与神经炎性斑块相关的YFP标记的膨体中异常积累。除了对Aβ对轴突和树突结构的影响进行表征外,Tg小鼠中YFP标记的神经元应该被证明是一种有价值的工具,可用于解释其他标记物的定位模式,并用于未来研究在体外和体内的活体组织中各种疾病状态下轴突和树突的动态变化。