Absence of synaptophysin near cortical neurons containing oligomer Aβ in Alzheimer's disease brain
Absence of synaptophysin near cortical neurons containing oligomer Aβ in Alzheimer's disease brain
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DOI：
10.1002/jnr.20952
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发表时间：
2006-08-15
影响因子：
4.2
通讯作者：
Mori, Hiroshi
中科院分区：
文献类型：
--
作者：
Ishibashi, Ken-Ichi;Tomiyama, Takami;Mori, Hiroshi
可溶性淀粉样β蛋白（A β）寡聚体最近被认为是导致阿尔茨海默病（AD）脑中老年斑形成之前的认知功能障碍的原因。通过使用新制备的针对寡聚体A β的抗体，而不是纤维状或单体A β，我们观察到AD脑中的寡聚体A β以不同于老年斑的方式定位为神经元中的点状免疫染色剂簇。由于寡聚体A β被广泛认为与突触失败有关，因此研究了寡聚体A β与突触素（一种突触分子标记物）的关系。我们观察到，免疫染色突触素缺乏附近的神经元轴承集群的寡聚体A β。本研究提供了形态学证据来支持这样的想法，即积累的寡聚体A β，而不是纤维状A β，与突触失败密切相关，这是认知功能障碍的主要原因。(c)2006 Wiley-Liss，Inc.
Soluble amyloid beta protein (A beta) oligomers have been considered recently to be responsible for the cognitive dysfunction that sets in prior to senile plaque formation in the Alzheimer's disease (AD) brain. By using the newly prepared antibody against oligomer A beta, rather than fibrillar or monomer A beta, we observed that oligomer A beta in AD brains was localized as clusters of dot-like immunostains in the neurons in a manner different from that in senile plaques. The relationship of oligomer A beta with synaptophysin, a synaptic molecular marker, was examined because oligomer A beta is widely believed to be related to synaptic failure. We observed that immunostainings for synaptophysin were absent near neurons bearing clusters of oligomer A beta. The present study provides morphological evidence to support the idea that accumulated oligomer A beta, but not fibrillar A beta, is closely associated with synaptic failure, which is the major cause of cognitive dysfunction. (c) 2006 Wiley-Liss, Inc.