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1
Nigral iron elevation is an invariable feature of Parkinson's disease and is a sufficient cause of neurodegeneration.黑质铁含量升高是帕金森病的一个恒定特征,并且是神经退行性变的一个充分原因。
Biomed Res Int. 2014;2014:581256. doi: 10.1155/2014/581256. Epub 2014 Jan 16.
2
Iron accumulation in Parkinson's disease.帕金森病中的铁积累。
J Neural Transm (Vienna). 2012 Dec;119(12):1511-4. doi: 10.1007/s00702-012-0905-9. Epub 2012 Oct 16.
3
Low plasma serotonin linked to higher nigral iron in Parkinson's disease.帕金森病患者血浆中低血清素与黑质铁含量升高有关。
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4
Parkinson's disease and iron.帕金森病与铁。
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5
Controversies about iron in parkinsonian and control substantia nigra.帕金森病患者与对照者黑质中铁元素的争议
Acta Neurobiol Exp (Wars). 1997;57(3):217-25. doi: 10.55782/ane-1997-1229.
6
Association of freezing of gait with nigral iron accumulation in patients with Parkinson's disease.帕金森病患者冻结步态与黑质铁蓄积的相关性。
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7
Investigations of differences in iron oxidation state inside single neurons from substantia nigra of Parkinson's disease and control patients using the micro-XANES technique.使用微X射线吸收近边结构(micro-XANES)技术对帕金森病患者和对照患者黑质单个神经元内铁氧化态差异进行的研究。
J Biol Inorg Chem. 2007 Feb;12(2):204-11. doi: 10.1007/s00775-006-0179-5. Epub 2006 Nov 21.
8
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J Synchrotron Radiat. 2001 Mar 1;8(Pt 2):998-1000. doi: 10.1107/s0909049500017726.
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Chronic expression of H-ferritin in dopaminergic midbrain neurons results in an age-related expansion of the labile iron pool and subsequent neurodegeneration: implications for Parkinson's disease.慢性表达 H 铁蛋白于多巴胺能中脑神经元可导致不稳定铁池随年龄增长而扩大,进而导致神经退行性变:对帕金森病的影响。
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Iron histochemistry of the substantia nigra in Parkinson's disease.帕金森病中黑质的铁组织化学
Neurodegeneration. 1994 Dec;3(4):277-82.

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Ferroptosis in central nervous system injuries: molecular mechanisms, diagnostic approaches, and therapeutic strategies.中枢神经系统损伤中的铁死亡:分子机制、诊断方法及治疗策略
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Midbrain and pallidal iron changes identify patients with REM sleep behaviour disorder and Parkinson's disease.中脑和苍白球铁含量变化可识别快速眼动睡眠行为障碍和帕金森病患者。
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Physiological Roles of Eumelanin- and Melanogenesis-Associated Diseases: A Look at the Potentialities of Engineered and Microbial Eumelanin in Clinical Practice.真黑素及黑素生成相关疾病的生理作用:审视工程化真黑素和微生物真黑素在临床实践中的潜力
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本文引用的文献

1
Targeting chelatable iron as a therapeutic modality in Parkinson's disease.将可螯合铁作为帕金森病的一种治疗方式
Antioxid Redox Signal. 2014 Jul 10;21(2):195-210. doi: 10.1089/ars.2013.5593. Epub 2014 Feb 6.
2
A delicate balance: Iron metabolism and diseases of the brain.微妙的平衡:铁代谢与脑部疾病。
Front Aging Neurosci. 2013 Jul 18;5:34. doi: 10.3389/fnagi.2013.00034. eCollection 2013.
3
Is R2* a new MRI biomarker for the progression of Parkinson's disease? A longitudinal follow-up.R2* 是否为帕金森病进展的新 MRI 生物标志物?一项纵向随访研究。
PLoS One. 2013;8(3):e57904. doi: 10.1371/journal.pone.0057904. Epub 2013 Mar 1.
4
Ceruloplasmin dysfunction and therapeutic potential for Parkinson disease.铜蓝蛋白功能障碍与帕金森病的治疗潜力。
Ann Neurol. 2013 Apr;73(4):554-9. doi: 10.1002/ana.23817. Epub 2013 Feb 19.
5
Stable iron isotope tracing reveals significant brain iron uptake in adult rats.稳定铁同位素示踪显示成年大鼠大脑中铁的摄取量显著增加。
Metallomics. 2013 Feb;5(2):167-73. doi: 10.1039/c2mt20226c.
6
Metallostasis in Alzheimer's disease.阿尔茨海默病中的金属稳态失衡。
Free Radic Biol Med. 2013 Sep;62:76-89. doi: 10.1016/j.freeradbiomed.2012.10.558. Epub 2012 Nov 9.
7
Nigral iron deposition occurs across motor phenotypes of Parkinson's disease.黑质铁沉积发生在帕金森病的各种运动表型中。
Eur J Neurol. 2012 Jul;19(7):969-76. doi: 10.1111/j.1468-1331.2011.03658.x. Epub 2012 Jan 30.
8
Tau deficiency induces parkinsonism with dementia by impairing APP-mediated iron export.tau 蛋白缺失通过损害 APP 介导体铁输出而诱导帕金森病伴痴呆。
Nat Med. 2012 Jan 29;18(2):291-5. doi: 10.1038/nm.2613.
9
Ceruloplasmin oxidation, a feature of Parkinson's disease CSF, inhibits ferroxidase activity and promotes cellular iron retention.血浆铜蓝蛋白氧化,帕金森病 CSF 的一个特征,抑制了亚铁氧化酶的活性并促进了细胞内铁的蓄积。
J Neurosci. 2011 Dec 14;31(50):18568-77. doi: 10.1523/JNEUROSCI.3768-11.2011.
10
Enlarged substantia nigra hyperechogenicity and risk for Parkinson disease: a 37-month 3-center study of 1847 older persons.黑质回声增强与帕金森病风险:一项针对1847名老年人的为期37个月的三中心研究
Arch Neurol. 2011 Jul;68(7):932-7. doi: 10.1001/archneurol.2011.141.

黑质铁含量升高是帕金森病的一个恒定特征,并且是神经退行性变的一个充分原因。

Nigral iron elevation is an invariable feature of Parkinson's disease and is a sufficient cause of neurodegeneration.

作者信息

Ayton Scott, Lei Peng

机构信息

The Florey Institute of Neuroscience and Mental Health, University of Melbourne, Kenneth Myer Building at Genetics Lane on Royal Parade, Parkville, VIC 3010, Australia.

出版信息

Biomed Res Int. 2014;2014:581256. doi: 10.1155/2014/581256. Epub 2014 Jan 16.

DOI:10.1155/2014/581256
PMID:24527451
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3914334/
Abstract

Parkinson's disease (PD) is a neurodegenerative disorder characterized by motor deficits accompanying degeneration of substantia nigra pars compactor (SNc) neurons. Although familial forms of the disease exist, the cause of sporadic PD is unknown. Symptomatic treatments are available for PD, but there are no disease modifying therapies. While the neurodegenerative processes in PD may be multifactorial, this paper will review the evidence that prooxidant iron elevation in the SNc is an invariable feature of sporadic and familial PD forms, participates in the disease mechanism, and presents as a tractable target for a disease modifying therapy.

摘要

帕金森病(PD)是一种神经退行性疾病,其特征是随着黑质致密部(SNc)神经元变性而出现运动功能障碍。尽管存在该疾病的家族性形式,但散发性PD的病因尚不清楚。目前有针对PD的对症治疗方法,但尚无改变疾病进程的疗法。虽然PD中的神经退行性过程可能是多因素的,但本文将综述相关证据,即SNc中促氧化剂铁水平升高是散发性和家族性PD形式的一个不变特征,参与疾病机制,并作为改变疾病进程疗法的一个可处理靶点。