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[阿尔茨海默型老年痴呆边缘叶变性进展的神经病理学研究]

[Neuropathological study on progression of the limbic degeneration in senile dementia of Alzheimer type].

作者信息

Kasahara M, Mizutani T

机构信息

Komagino Hospital, Tokyo, Japan.

出版信息

No To Shinkei. 1997 Jan;49(1):51-8.

PMID:9027902
Abstract

Neuropathological study on the limbic lesion of 33 autopsy cases with senile dementia of Alzheimer type (SDAT) showed as follows. 1) The entorhinal cortex was more atrophied than the hippocampus. 2) Neuronal loss was found in the 2nd and 3rd layers of the entorhinal cortex, irrespective of the different numbers of senile plaques and neurofibrillary tangles (NFTs). 3) Fibrillary gliosis occurred in the stratum lacunosum of the hippocampus, irrespective of the different degrees of neuronal loss in the stratum pyramidale of the hippocampus. 4) The prosubiculum showed gliosis disproportional to neuronal loss. 5) The degree of fibrillary gliosis in the stratum lacunosum of the hippocampus and in the prosubiculum was proportional to that of the entorhinal cortical degeneration. 6) The shape of the hippocampus of the cases with SDAT was different from that in the cases with anoxic encephalopathy in which neuronal loss in the CA1 occurred primarily: 7) Distribution pattern of the lesion in the hippocampus of SDAT cases was almost the same as that found in the cases with infarct in the collateral sulcus involving the entorhinal cortex. It is assumed that the hippocampal atrophy is a primary degeneration attributable to appearance of senile plaques and NFTs. However, our present observations and previous report (Neurosci Lett 184: 141-144 1995) suggest that degeneration of the entorhinal cortex and its efferent fibres (perforant pathway) plays a considerable part of role in development of the hippocampal atrophy. The present study could contribute to understanding of progression of the limbic lesion in SDAT.

摘要

对33例阿尔茨海默型老年痴呆(SDAT)尸检病例的边缘系统病变进行的神经病理学研究结果如下:1)内嗅皮质比海马萎缩更严重。2)在内嗅皮质的第2层和第3层发现神经元丢失,与老年斑和神经原纤维缠结(NFTs)数量的差异无关。3)海马腔隙层出现纤维性胶质增生,与海马锥体层神经元丢失程度的差异无关。4)前下托显示胶质增生与神经元丢失不成比例。5)海马腔隙层和前下托的纤维性胶质增生程度与内嗅皮质变性程度成正比。6)SDAT病例的海马形状与主要发生CA1区神经元丢失的缺氧性脑病病例不同。7)SDAT病例海马病变的分布模式与累及内嗅皮质的侧副沟梗死病例几乎相同。据推测,海马萎缩是由老年斑和NFTs出现导致的原发性变性。然而,我们目前的观察结果和之前的报告(《神经科学快报》184: 141 - 144,1995年)表明,内嗅皮质及其传出纤维(穿通通路)的变性在海马萎缩的发展中起了相当大的作用。本研究有助于理解SDAT中边缘系统病变的进展。

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