病例-报告:一过性脑缺血发作后抑郁症患者基因表达异常,经神经生理神经标记物证实。

M. Trystuła, M. Żychowska, M. Wilk-Frańczuk, J. Kropotov, M. Pąchalska
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引用次数: 3

摘要

本研究的目的是通过使用定量脑电图和事件相关电位,评估与“预警卒中”后抑郁症患者细胞应激反应相关的基因表达失调,该患者的神经生理神经标记物的存在证实了这一点。与健康对照组的基因表达相比,对患者进行了7种与应激反应相关的基因检测:HSPA1A、HSPB1、IL6、IL10、CRP、HSF-1以及NF-κB。一名54岁的患者,既往有精神分裂症(20岁)、短暂性脑缺血发作(53岁)和抑郁症病史,经功能、认知、情感和情感诊断证实,接受了与应激反应相关基因表达的额外检测。检测热休克蛋白(HSPA1A, HSPB1)、白细胞介素(IL6, IL10)和c反应蛋白编码基因的表达以及调节其表达的因子。对该患者进行的测试结果与42名健康对照者进行了比较。诊断测试显示这些基因的表达上调,表现为靶基因和调控基因的表达增加。“预警卒中”后的抑郁障碍似乎与编码热休克蛋白和白细胞介素的基因过度表达有关。对更大人群的进一步研究可能为改进治疗方法提供依据。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
CASE-REPORT Dysregulation of gene expression in a patient with depressive disorder after transient ischemic attack confirmed by a neurophysiological neuromarker.
The aim of this study was to evaluate dysregulation of gene expression associated with the cellular stress response in a patient with a post-"warning stroke" depressive disorder confirmed by the presence of a neurophysiological neuromarker through the use of quantitative EEG and event-related potentials. The patient was tested for seven genes associated with the stress reaction: HSPA1A, HSPB1, IL6, IL10, CRP, and HSF-1 along with NF-κB, compared to gene expression in health controls. A 54-year-old patient with a past history of schizophrenia (at the age of 20), and of transient ischemic attack (at the age of 53) and depressive disorder confirmed by functional, cognitive, emotional, and affectional diagnostics underwent additional testing for expression of the genes associated with stress response. The expression of genes coding for heat shock protein (HSPA1A, HSPB1), interleukins (IL6, IL10), and C-reactive protein was tested along with factors that regulate their expression. The results of the tests conducted on this patient were compared with 42 healthy control subjects. Diagnostic testing revealed upregulation in expression of these genes, presenting as increased expression of the target genes and of the regulatory genes. A post-"warning stroke" depressive disorder appears to be associated with overexpression of the genes coding for HSP and interleukins. Further research on larger groups of people may provide grounds for treatment modification.
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