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1
Parkin disease and the Lewy body conundrum.帕金森病与路易体难题。
Mov Disord. 2013 Jun;28(6):702-4. doi: 10.1002/mds.25486. Epub 2013 May 7.
2
Lewy body pathology and typical Parkinson disease in a patient with a heterozygous (R275W) mutation in the Parkin gene (PARK2).一名携带帕金基因(PARK2)杂合(R275W)突变的患者出现路易体病理改变及典型帕金森病。
Acta Neuropathol. 2012 Jun;123(6):901-3. doi: 10.1007/s00401-012-0991-7. Epub 2012 May 4.
3
Comment on "S-nitrosylation of parkin regulates ubiquitination and compromises parkin's protective function".对“帕金蛋白的S-亚硝基化调节泛素化并损害帕金蛋白的保护功能”的评论
Science. 2005 Jun 24;308(5730):1870; author reply 1870. doi: 10.1126/science.1110353.
4
Parkin mediates nonclassical, proteasomal-independent ubiquitination of synphilin-1: implications for Lewy body formation.帕金介导突触核蛋白-1的非经典、蛋白酶体非依赖性泛素化:对路易小体形成的影响。
J Neurosci. 2005 Feb 23;25(8):2002-9. doi: 10.1523/JNEUROSCI.4474-04.2005.
5
The parkin-like human homolog of Drosophila ariadne-1 (HHARI) can induce aggresome formation in mammalian cells and is immunologically detectable in Lewy bodies.果蝇 ariadne-1(HHARI)的人 parkin 样同源物可在哺乳动物细胞中诱导聚集物形成,并可在路易小体中免疫检测到。
J Mol Neurosci. 2012 Jan;46(1):109-21. doi: 10.1007/s12031-011-9535-1. Epub 2011 May 18.
6
Inclusion body formation and neurodegeneration are parkin independent in a mouse model of alpha-synucleinopathy.在α-突触核蛋白病小鼠模型中,包涵体形成和神经退行性变与帕金蛋白无关。
J Neurosci. 2006 Apr 5;26(14):3685-96. doi: 10.1523/JNEUROSCI.0414-06.2006.
7
Regulation of parkin and PINK1 by neddylation.Parkin 和 PINK1 的泛素化调节。
Hum Mol Genet. 2012 Jun 1;21(11):2514-23. doi: 10.1093/hmg/dds070. Epub 2012 Mar 2.
8
Ubiquitin-proteasome system and Parkinson's diseases.泛素-蛋白酶体系统与帕金森病
Exp Neurol. 2005 Feb;191 Suppl 1:S17-27. doi: 10.1016/j.expneurol.2004.08.021.
9
Parkin ubiquitinates the alpha-synuclein-interacting protein, synphilin-1: implications for Lewy-body formation in Parkinson disease.帕金蛋白使与α-突触核蛋白相互作用的蛋白——突触结合蛋白1发生泛素化:对帕金森病路易小体形成的影响
Nat Med. 2001 Oct;7(10):1144-50. doi: 10.1038/nm1001-1144.
10
Parkin localizes to the Lewy bodies of Parkinson disease and dementia with Lewy bodies.帕金蛋白定位于帕金森病和路易体痴呆的路易小体中。
Am J Pathol. 2002 May;160(5):1655-67. doi: 10.1016/S0002-9440(10)61113-3.

引用本文的文献

1
Cutaneous nerve fiber pathology and function in Parkinson's disease and atypical parkinsonism - a cohort study.帕金森病和非典型帕金森综合征的皮肤神经纤维病理学与功能——一项队列研究
NPJ Parkinsons Dis. 2025 Jun 15;11(1):170. doi: 10.1038/s41531-025-01030-y.
2
A personalised and comprehensive approach is required to suppress or replenish SNCA for Parkinson's disease.需要一种个性化且全面的方法来抑制或补充帕金森病中的α-突触核蛋白(SNCA)。
NPJ Parkinsons Dis. 2025 Mar 4;11(1):42. doi: 10.1038/s41531-025-00887-3.
3
Physiological roles of α-synuclein serine-129 phosphorylation - not an oxymoron.α-突触核蛋白丝氨酸 129 磷酸化的生理作用——并非矛盾。
Trends Neurosci. 2024 Jul;47(7):480-490. doi: 10.1016/j.tins.2024.05.005. Epub 2024 Jun 10.
4
Early-Onset Parkinson's Disease: Creating the Right Environment for a Genetic Disorder.早发性帕金森病:为遗传疾病创造合适的环境。
J Parkinsons Dis. 2022;12(8):2353-2367. doi: 10.3233/JPD-223380.
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Human Induced Pluripotent Stem Cell Phenotyping and Preclinical Modeling of Familial Parkinson's Disease.人类诱导多能干细胞表型分析及家族性帕金森病的临床前建模。
Genes (Basel). 2022 Oct 25;13(11):1937. doi: 10.3390/genes13111937.
6
Precision Medicine in Parkinson's Disease: From Genetic Risk Signals to Personalized Therapy.帕金森病的精准医学:从遗传风险信号到个性化治疗
Brain Sci. 2022 Sep 28;12(10):1308. doi: 10.3390/brainsci12101308.
7
Targeted Molecular Therapeutics for Parkinson's Disease: A Role for Antisense Oligonucleotides?帕金森病的靶向分子疗法:反义寡核苷酸的作用?
Mov Disord. 2022 Nov;37(11):2184-2190. doi: 10.1002/mds.29201. Epub 2022 Aug 29.
8
Roles of α-Synuclein and Disease-Associated Factors in Models of Parkinson's Disease.α-突触核蛋白与疾病相关因子在帕金森病模型中的作用。
Int J Mol Sci. 2022 Jan 28;23(3):1519. doi: 10.3390/ijms23031519.
9
Therapeutic Potential of -Synuclein Evolvability for Autosomal Recessive Parkinson's Disease.α-突触核蛋白可进化性在常染色体隐性帕金森病中的治疗潜力
Parkinsons Dis. 2021 Nov 23;2021:6318067. doi: 10.1155/2021/6318067. eCollection 2021.
10
The Promise of the Zebrafish Model for Parkinson's Disease: Today's Science and Tomorrow's Treatment.斑马鱼模型对帕金森病的前景:当今的科学与未来的治疗
Front Genet. 2021 Apr 15;12:655550. doi: 10.3389/fgene.2021.655550. eCollection 2021.

本文引用的文献

1
A Peruvian family with a novel PARK2 mutation: Clinical and pathological characteristics.一个携带新型PARK2突变的秘鲁家庭:临床和病理特征
Parkinsonism Relat Disord. 2015 May;21(5):444-8. doi: 10.1016/j.parkreldis.2015.01.005. Epub 2015 Jan 15.
2
Parkin disease: a clinicopathologic entity?帕金森病:一种临床病理实体?
JAMA Neurol. 2013 May;70(5):571-9. doi: 10.1001/jamaneurol.2013.172.
3
Lewy body pathology in a patient with a homozygous parkin deletion.路易体病理改变见于一名纯合子 parkin 缺失患者。
Mov Disord. 2013 Mar;28(3):388-91. doi: 10.1002/mds.25346. Epub 2013 Feb 11.
4
The neuropathology of genetic Parkinson's disease.遗传帕金森病的神经病理学。
Mov Disord. 2012 Jun;27(7):831-42. doi: 10.1002/mds.24962. Epub 2012 Mar 26.
5
Mitophagy and Parkinson's disease: the PINK1-parkin link.线粒体自噬与帕金森病:PINK1-帕金蛋白联系
Biochim Biophys Acta. 2011 Apr;1813(4):623-33. doi: 10.1016/j.bbamcr.2010.08.007. Epub 2010 Aug 21.
6
PINK1-linked parkinsonism is associated with Lewy body pathology.PINK1 相关性帕金森病与路易体病理相关。
Brain. 2010 Apr;133(Pt 4):1128-42. doi: 10.1093/brain/awq051. Epub 2010 Mar 30.
7
Lewy body pathology in normal elderly subjects.正常老年受试者中的路易体病理改变。
J Neuropathol Exp Neurol. 2009 Jul;68(7):816-22. doi: 10.1097/NEN.0b013e3181ac10a7.
8
Clinical, pathologic and genetic studies on autosomal recessive early-onset parkinsonism with diurnal fluctuation.
Parkinsonism Relat Disord. 1998 Aug;4(2):65-72. doi: 10.1016/s1353-8020(98)00015-7.
9
Obligatory role for complex I inhibition in the dopaminergic neurotoxicity of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP).复合体I抑制在1-甲基-4-苯基-1,2,3,6-四氢吡啶(MPTP)多巴胺能神经毒性中的关键作用。
Toxicol Sci. 2007 Jan;95(1):196-204. doi: 10.1093/toxsci/kfl133. Epub 2006 Oct 12.
10
Heterogeneous phenotype in a family with compound heterozygous parkin gene mutations.一个患有复合杂合性帕金基因突变的家族中的异质性表型。
Arch Neurol. 2006 Feb;63(2):273-7. doi: 10.1001/archneur.63.2.273.

Parkin disease and the Lewy body conundrum.

作者信息

Doherty Karen M, Hardy John

机构信息

Reta Lila Weston Institute of Neurological Studies and Research Laboratories, Department of Molecular Neuroscience, University College London Institute of Neurology, London, United Kingdom.

出版信息

Mov Disord. 2013 Jun;28(6):702-4. doi: 10.1002/mds.25486. Epub 2013 May 7.

DOI:10.1002/mds.25486
PMID:23653422
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3739929/
Abstract
摘要