Posterior parahippocampal gyrus pathology in Alzheimer's disease
Posterior parahippocampal gyrus pathology in Alzheimer's disease
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DOI：
10.1016/j.neuroscience.2008.03.077
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发表时间：
2008-06-23
期刊：
影响因子：
3.3
通讯作者：
Zaheer, A.
中科院分区：
文献类型：
--
作者：
Thangavel, R.;Van Hoesen, G. W.;Zaheer, A.
非人类灵长类动物脑的海马旁后回（PPHG）在皮质神经系统中具有明显的双重作用。一方面，它是向内嗅皮层和海马结构提供皮层输入的关键环节，而另一方面，它接收来自这些结构的输出，并通过将内侧颞叶输出传播到皮层而广泛投射。TF和TH区的第三层主要介导前者（输入），而第五层介导后者（输出）。我们用病理染色（Nissl，Thioflavin S）和表型特异性染色（非磷酸化神经丝蛋白（SM 132）和小清蛋白（PV））检测了正常人脑和阿尔茨海默病（AD）的TF和TH区。沿着研究了7例临床和病理证实的AD病例以及6例年龄匹配的正常病例。我们的观察结果表明，神经纤维缠结（NFTs）大量投资的TF和TH神经元，形成第三层和第五层在这两个皮质区，大金字塔，形成第五层包含更多的NFTs。这些变化，以及可能的锥体细胞丢失，极大地改变了细胞结构图，并减少了SM132染色模式。TH区的第III层失去了大部分的SM132免疫反应性，而这种变化在TF区的第V层更明显。两个区域的PV染色基本上不受影响。正常病例不含病理学或细胞结构改变的证据。这些观察结果揭示了AD中与记忆相关的时间神经系统的进一步破坏，其中病理学选择性地改变了海马结构的输入及其到皮层的输出。由Elsevier Ltd代表IBRO出版。
The posterior parahippocampal gyrus (PPHG) of the non-human primate brain has a distinct dual role in cortical neural systems. On the one hand, it is a critical link in providing the entorhinal cortex and hippocampal formation with cortical input, while on the other hand it receives output from these structures and projects widely by disseminating the medial temporal lobe output to the cortex. Layer III of TF and TH areas largely mediate the former (input) while layer V mediates the latter (output). We have examined areas TF and TH in the normal human brain and in Alzheimer's disease (AD) using pathological stains (Nissl, Thioflavin S) and phenotype specific stains non-phosphorylated neurofilament protein (SM132) and parvalbumin (PV). Seven clinically and pathologically confirmed AD cases have been studied along with six age-compatible normal cases. Our observations reveal that neurofibrillary tangles (NFTs) heavily invest the area TF and TH neurons that form layers III and V. In both cortical areas, the large pyramids that form layer V contain a greater number of NFTs. These changes, and possibly, pyramidal cell loss, greatly alter the cytoarchitectural picture and diminish SM132 staining patterns. Layer III of area TH loses the majority of SM132 immunoreactivity, whereas this change is more conspicuous in layer V of area TF. PV-staining in both areas is largely unaffected. Normal cases contained no evidence of pathology or altered cytoarchitecture. These observations reveal a further disruption of memory-related temporal neural systems in AD where pathology selectively alters both the input to the hippocampal formation and its output to the cortex. Published by Elsevier Ltd on behalf of IBRO.