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精神分裂症患者颞叶中少突胶质细胞糖蛋白的神经病理学研究。

The neuropathological study of myelin oligodendrocyte glycoprotein in the temporal lobe of schizophrenia patients.

机构信息

1Department of Psychiatry,Graduate School of Medicine,Nagoya University,Showa-ku,Nagoya,Aichi,Japan.

2Department of Psychiatry,Tokyo Metropolitan Matsuzawa Hospital,Setagaya-ku,Tokyo,Japan.

出版信息

Acta Neuropsychiatr. 2018 Aug;30(4):232-240. doi: 10.1017/neu.2018.6. Epub 2018 Mar 22.

DOI:10.1017/neu.2018.6
PMID:29564992
Abstract

OBJECTIVE

Recent studies based on the neuroimaging analysis, genomic analysis and transcriptome analysis of the postmortem brain suggest that the pathogenesis of schizophrenia is related to myelin-oligodendrocyte abnormalities. However, no serious neuropathological investigation of this protein in the schizophrenic brain has yet been performed. In this study, to confirm the change in neuropathological findings due to the pathogenesis of this disease, we observed the expression of myelin-oligodendrocyte directly in the brain tissue of schizophrenia patients.

METHODS

Myelin oligodendrocyte glycoprotein (MOG) was evaluated in the cortex of the superior temporal gyrus (STG) and the hippocampus in 10 schizophrenic and nine age- and sex-matched normal control postmortem brains.

RESULTS

The expression of MOG was significantly lower in the middle layer of the neocortex of the STG and stratum lucidum of CA3 in the hippocampus in the long-term schizophrenic brains (patients with ≥30 years of illness duration) than in the age-matched controls. Furthermore, the thickness of MOG-positive fibre-like structures was significantly lower in both regions of the long-term schizophrenic brains than in the age-matched controls.

CONCLUSION

These findings suggest that a long duration of illness has a marked effect on the expression of MOG in these regions, and that myelin-oligodendrocyte abnormalities in these regions may be related to the progressive pathophysiology of schizophrenia.

摘要

目的

最近基于对死后大脑的神经影像学分析、基因组分析和转录组分析的研究表明,精神分裂症的发病机制与髓鞘少突胶质细胞异常有关。然而,尚未对精神分裂症大脑中这种蛋白质进行严重的神经病理学研究。在这项研究中,为了证实该疾病发病机制导致的神经病理学变化,我们直接观察了精神分裂症患者脑组织中髓鞘少突胶质细胞的表达。

方法

在 10 例精神分裂症和 9 例年龄和性别匹配的正常对照死后大脑的颞上回(STG)皮质和海马中评估了髓鞘少突胶质细胞糖蛋白(MOG)。

结果

长期精神分裂症患者(患病≥30 年)的 STG 新皮质中层和海马 CA3 层状亮区的 MOG 表达明显低于年龄匹配的对照组。此外,长期精神分裂症患者这两个区域的 MOG 阳性纤维样结构的厚度明显低于年龄匹配的对照组。

结论

这些发现表明,疾病的长期病程对这些区域 MOG 的表达有显著影响,这些区域的髓鞘少突胶质细胞异常可能与精神分裂症的进行性病理生理学有关。

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