• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

伴有路易小体病的个体的氧化应激和线粒体功能指标

Indices of oxidative stress and mitochondrial function in individuals with incidental Lewy body disease.

作者信息

Dexter D T, Sian J, Rose S, Hindmarsh J G, Mann V M, Cooper J M, Wells F R, Daniel S E, Lees A J, Schapira A H

机构信息

Parkinson's Disease Society Experimental Research Laboratories, King's College London, United Kingdom.

出版信息

Ann Neurol. 1994 Jan;35(1):38-44. doi: 10.1002/ana.410350107.

DOI:10.1002/ana.410350107
PMID:8285590
Abstract

Brain tissue from normal individuals with incidental Lewy bodies and cell loss in pigmented substantia nigra neurons (asymptomatic Parkinson's disease) and age-matched control subjects without nigral Lewy bodies was examined biochemically. There was no difference in dopamine levels or dopamine turnover in the caudate and putamen of individuals with incidental Lewy body disease compared to control subjects. There were no differences in levels of iron, copper, manganese, or zinc in the substantia nigra or other brain regions from the individuals with incidental Lewy body disease compared to those from control subjects. Similarly, ferritin levels in the substantia nigra and other brain areas were unaltered. There was no difference in the activity of succinate cytochrome c reductase (complexes II and III) or cytochrome oxidase (complex IV) between incidental Lewy body subjects and control subjects. Rotenone-sensitive NADH coenzyme Q1 reductase activity (complex I) was reduced to levels intermediate between those in control subjects and those in patients with overt Parkinson's disease, but this change did not reach statistical significance. The levels of reduced glutathione in substantia nigra were reduced by 35% in patients with incidental Lewy body disease compared to control subjects. Reduced glutathione levels in other brain regions were unaffected and there were no changes in oxidized glutathione levels in any brain region. Altered iron metabolism is not detectable in the early stages of nigral dopamine cell degeneration. There may be some impairment of mitochondrial complex I activity in the substantia nigra in Parkinson's disease.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

对有偶发性路易小体且黑质色素神经元有细胞丢失的正常个体(无症状帕金森病)以及年龄匹配的无黑质路易小体的对照受试者的脑组织进行了生化检查。与对照受试者相比,有偶发性路易小体病的个体尾状核和壳核中的多巴胺水平或多巴胺周转率没有差异。与对照受试者相比,有偶发性路易小体病的个体黑质或其他脑区中的铁、铜、锰或锌水平没有差异。同样,黑质和其他脑区的铁蛋白水平未改变。偶发性路易小体受试者和对照受试者之间的琥珀酸细胞色素c还原酶(复合体II和III)或细胞色素氧化酶(复合体IV)活性没有差异。鱼藤酮敏感的NADH辅酶Q1还原酶活性(复合体I)降至对照受试者和明显帕金森病患者之间的中间水平,但这种变化未达到统计学意义。与对照受试者相比,有偶发性路易小体病的患者黑质中还原型谷胱甘肽水平降低了35%。其他脑区的还原型谷胱甘肽水平未受影响,任何脑区的氧化型谷胱甘肽水平均无变化。在黑质多巴胺细胞变性的早期阶段未检测到铁代谢改变。帕金森病患者黑质中的线粒体复合体I活性可能存在一些损害。(摘要截短至250字)

相似文献

1
Indices of oxidative stress and mitochondrial function in individuals with incidental Lewy body disease.伴有路易小体病的个体的氧化应激和线粒体功能指标
Ann Neurol. 1994 Jan;35(1):38-44. doi: 10.1002/ana.410350107.
2
Alpha-synuclein redistributes to neuromelanin lipid in the substantia nigra early in Parkinson's disease.在帕金森病早期,α-突触核蛋白重新分布至黑质中的神经黑素脂质。
Brain. 2005 Nov;128(Pt 11):2654-64. doi: 10.1093/brain/awh584. Epub 2005 Jul 6.
3
Alterations in glutathione levels in Parkinson's disease and other neurodegenerative disorders affecting basal ganglia.帕金森病及其他影响基底神经节的神经退行性疾病中谷胱甘肽水平的改变。
Ann Neurol. 1994 Sep;36(3):348-55. doi: 10.1002/ana.410360305.
4
Presymptomatic detection of Parkinson's disease.帕金森病的症状前检测
J Neural Transm Suppl. 1993;40:23-36.
5
What process causes nigral cell death in Parkinson's disease?帕金森病中黑质细胞死亡是由什么过程导致的?
Neurol Clin. 1992 May;10(2):387-403.
6
Complex I, iron, and ferritin in Parkinson's disease substantia nigra.帕金森病黑质中的复合体I、铁和铁蛋白。
Ann Neurol. 1994 Dec;36(6):876-81. doi: 10.1002/ana.410360612.
7
Neurofilament mRNA is reduced in Parkinson's disease substantia nigra pars compacta neurons.帕金森病黑质致密部神经元中的神经丝信使核糖核酸减少。
J Comp Neurol. 1993 Mar 15;329(3):328-36. doi: 10.1002/cne.903290304.
8
[Incidental occurrence of Lewy bodies in the brains of elderly patients--the relevance to aging and Parkinson's disease].[老年患者大脑中路易小体的偶然出现——与衰老及帕金森病的相关性]
No To Shinkei. 1993 Nov;45(11):1033-8.
9
ELISA reveals a difference in the structure of substantia nigra ferritin in Parkinson's disease and incidental Lewy body compared to control.酶联免疫吸附测定显示,与对照组相比,帕金森病和路易小体病患者黑质铁蛋白的结构存在差异。
Parkinsonism Relat Disord. 2007 May;13(4):214-8. doi: 10.1016/j.parkreldis.2006.10.002. Epub 2007 Feb 1.
10
Decreased serum ceruloplasmin levels characteristically aggravate nigral iron deposition in Parkinson's disease.血清铜蓝蛋白水平降低特征性地加重帕金森病患者的黑质铁沉积。
Brain. 2011 Jan;134(Pt 1):50-8. doi: 10.1093/brain/awq319. Epub 2010 Nov 24.

引用本文的文献

1
Metabolic Dysfunction in Parkinson's Disease: Unraveling the Glucose-Lipid Connection.帕金森病中的代谢功能障碍:揭示葡萄糖 - 脂质关联
Biomedicines. 2024 Dec 13;12(12):2841. doi: 10.3390/biomedicines12122841.
2
Postencephalitic Parkinsonism: Unique Pathological and Clinical Features-Preliminary Data.脑炎后帕金森病:独特的病理和临床特征——初步数据。
Cells. 2024 Sep 10;13(18):1511. doi: 10.3390/cells13181511.
3
Metallomic analysis of brain tissues distinguishes between cases of dementia with Lewy bodies, Alzheimer's disease, and Parkinson's disease dementia.
脑组织的金属组学分析可区分路易体痴呆、阿尔茨海默病和帕金森病痴呆病例。
Front Neurosci. 2024 Jun 26;18:1412356. doi: 10.3389/fnins.2024.1412356. eCollection 2024.
4
Neuroprotective effects of coenzyme Q10 on neurological diseases: a review article.辅酶Q10对神经疾病的神经保护作用:一篇综述文章。
Front Neurosci. 2023 Jun 23;17:1188839. doi: 10.3389/fnins.2023.1188839. eCollection 2023.
5
A beginner's guide into curated analyses of open access datasets for biomarker discovery in neurodegeneration.生物标志物发现的开放获取数据集策展分析入门指南。
Sci Data. 2023 Jul 6;10(1):432. doi: 10.1038/s41597-023-02338-1.
6
The vicious circle between homocysteine, methyl group-donating vitamins and chronic levodopa intake in Parkinson's disease.同型半胱氨酸、供甲基维生素与慢性左旋多巴摄入在帕金森病中的恶性循环。
J Neural Transm (Vienna). 2024 Jun;131(6):631-638. doi: 10.1007/s00702-023-02666-x. Epub 2023 Jun 17.
7
Lewy bodies, iron, inflammation and neuromelanin: pathological aspects underlying Parkinson's disease.路易体、铁、炎症和神经黑色素:帕金森病的病理基础。
J Neural Transm (Vienna). 2023 May;130(5):627-646. doi: 10.1007/s00702-023-02630-9. Epub 2023 Apr 16.
8
Redox dysregulation as a driver for DNA damage and its relationship to neurodegenerative diseases.氧化还原失调作为 DNA 损伤的驱动因素及其与神经退行性疾病的关系。
Transl Neurodegener. 2023 Apr 14;12(1):18. doi: 10.1186/s40035-023-00350-4.
9
AMPK-dependent autophagy activation and alpha-Synuclein clearance: a putative mechanism behind alpha-mangostin's neuroprotection in a rotenone-induced mouse model of Parkinson's disease.AMPK 依赖性自噬激活和 alpha-突触核蛋白清除:芒果苷在鱼藤酮诱导的帕金森病小鼠模型中神经保护作用的潜在机制。
Metab Brain Dis. 2022 Dec;37(8):2853-2870. doi: 10.1007/s11011-022-01087-1. Epub 2022 Sep 30.
10
Harnessing the Therapeutic Potential of the Nrf2/Bach1 Signaling Pathway in Parkinson's Disease.挖掘Nrf2/Bach1信号通路在帕金森病中的治疗潜力
Antioxidants (Basel). 2022 Sep 9;11(9):1780. doi: 10.3390/antiox11091780.