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帕金森病黑质中细胞色素c氧化酶的缺陷:一项免疫组织化学和形态计量学研究。

Defects of cytochrome c oxidase in the substantia nigra of Parkinson's disease: and immunohistochemical and morphometric study.

作者信息

Itoh K, Weis S, Mehraein P, Müller-Höcker J

机构信息

Institute of Neuropathology, Ludwig-Maximilians-University, Munich, Germany.

出版信息

Mov Disord. 1997 Jan;12(1):9-16. doi: 10.1002/mds.870120104.

Abstract

Defects of respiratory chain complexes were considered as possible pathogenetic mechanisms in Parkinson's disease (PD). Changes of cytochrome c oxidase (COX) in four different nuclei of the substantia nigra of 8 PD cases and 10 age-matched controls were investigated by means of morphometry and immunohistochemistry. Pigmented neurons with COX defects were randomly distributed within the the four nuclei of PD cases, but only in the posterolateral nucleus was the numerical density of pigmented neurons with COX defects significantly increased compared with controls. The numerical density of pigmented neurons without COX defects was significantly reduced in the anteromedial, anterointermediolateral, and posterolateral nuclei in PD. The cell size of pigmented neurons with and without COX defects was significantly diminished in the anteromedial and posterolateral nuclei of PD cases. It is suggested that complex IV defects in nigral neurons are most probably a result of accelerated aging, but are least likely to be a primary aspect of the pathogenetic processes occurring in PD.

摘要

呼吸链复合物缺陷被认为是帕金森病(PD)可能的发病机制。通过形态计量学和免疫组织化学方法,研究了8例PD患者和10例年龄匹配对照者黑质四个不同核团中细胞色素c氧化酶(COX)的变化。PD患者中存在COX缺陷的色素神经元随机分布于四个核团内,但仅在后外侧核中,存在COX缺陷的色素神经元的数量密度与对照相比显著增加。PD患者中,在内侧前核、前中间外侧核和后外侧核中,不存在COX缺陷的色素神经元的数量密度显著降低。在PD患者的内侧前核和后外侧核中,存在和不存在COX缺陷的色素神经元的细胞大小均显著减小。提示黑质神经元中的复合物IV缺陷很可能是加速衰老的结果,但最不可能是PD发病过程的主要方面。

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