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帕金森病遗传缺陷动物模型的研究进展:特点与应用

Progress in Parkinson's disease animal models of genetic defects: Characteristics and application.

作者信息

Zhang Chutian, Chen Shiya, Li Xiyu, Xu Qian, Lin Yao, Lin Fan, Yuan Mingzhou, Zi Yong, Cai Jing

机构信息

Academy of Integrative Medicine, Fujian University of Traditional Chinese Medicine, Fuzhou, Fujian 350122, China.

The Third Affiliated People's Hospital of Fujian University of Traditional Chinese Medicine, Fuzhou, Fujian 350122, China.

出版信息

Biomed Pharmacother. 2022 Nov;155:113768. doi: 10.1016/j.biopha.2022.113768. Epub 2022 Sep 28.

DOI:10.1016/j.biopha.2022.113768
PMID:36182736
Abstract

Parkinson's disease (PD) is the second major progressive neurodegenerative disease, which critically impacts patients' quality of life. Based on genetics, animal models of genetic defects created by gene editing technology have clear advantages in reflecting PD's pathogenesis and pathological characteristics and exploring potential therapeutic targets for PD. In this review, we summarized animal models of genetic defects in various pathogenesis of PD, including α-synuclein abnormal encoding, autophagy-lysosome system defects, ubiquitin protease system defects, and mitochondria-related dysfunction, and discuss their respective advantages, limitations, and application directions to provide a reference for the application of animal models of PD and research on anti-PD therapy.

摘要

帕金森病(PD)是第二大主要的进行性神经退行性疾病,严重影响患者的生活质量。基于遗传学,利用基因编辑技术创建的基因缺陷动物模型在反映PD的发病机制和病理特征以及探索PD的潜在治疗靶点方面具有明显优势。在本综述中,我们总结了PD各种发病机制中的基因缺陷动物模型,包括α-突触核蛋白异常编码、自噬-溶酶体系统缺陷、泛素蛋白酶系统缺陷和线粒体相关功能障碍,并讨论了它们各自的优势、局限性和应用方向,为PD动物模型的应用及抗PD治疗研究提供参考。

相似文献

1
Progress in Parkinson's disease animal models of genetic defects: Characteristics and application.帕金森病遗传缺陷动物模型的研究进展:特点与应用
Biomed Pharmacother. 2022 Nov;155:113768. doi: 10.1016/j.biopha.2022.113768. Epub 2022 Sep 28.
2
How can rAAV-α-synuclein and the fibril α-synuclein models advance our understanding of Parkinson's disease?重组腺相关病毒-α-突触核蛋白和丝状α-突触核蛋白模型如何促进我们对帕金森病的理解?
J Neurochem. 2016 Oct;139 Suppl 1(Suppl 1):131-155. doi: 10.1111/jnc.13627. Epub 2016 May 4.
3
Genetic animal models of Parkinson's disease.帕金森病的遗传动物模型。
Neuron. 2010 Jun 10;66(5):646-61. doi: 10.1016/j.neuron.2010.04.034.
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The Overcrowded Crossroads: Mitochondria, Alpha-Synuclein, and the Endo-Lysosomal System Interaction in Parkinson's Disease.《拥挤的十字路口:帕金森病中线粒体、α-突触核蛋白与内溶酶体系统的相互作用》
Int J Mol Sci. 2019 Oct 25;20(21):5312. doi: 10.3390/ijms20215312.
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Progress in the pathogenesis and genetics of Parkinson's disease.帕金森病的发病机制与遗传学研究进展
Philos Trans R Soc Lond B Biol Sci. 2008 Jun 27;363(1500):2215-27. doi: 10.1098/rstb.2008.2273.
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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.
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Therapeutic strategies for Parkinson's disease based on data derived from genetic research.基于基因研究数据的帕金森病治疗策略
J Neurol. 2003 Feb;250 Suppl 1:I3-10. doi: 10.1007/s00415-003-1101-3.
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Mitochondrial dysfunction in genetic animal models of Parkinson's disease.帕金森病遗传动物模型中的线粒体功能障碍。
Antioxid Redox Signal. 2012 May 1;16(9):896-919. doi: 10.1089/ars.2011.4200. Epub 2011 Oct 4.
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[Etiology and pathogenesis of Parkinson's disease: from mitochondrial dysfunctions to familial Parkinson's disease].帕金森病的病因与发病机制:从线粒体功能障碍到家族性帕金森病
Rinsho Shinkeigaku. 2004 Apr-May;44(4-5):241-62.
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α-synuclein expression from a single copy transgene increases sensitivity to stress and accelerates neuronal loss in genetic models of Parkinson's disease.α-突触核蛋白的单拷贝转基因表达增加了对帕金森病遗传模型中应激的敏感性并加速了神经元的丢失。
Exp Neurol. 2018 Dec;310:58-69. doi: 10.1016/j.expneurol.2018.09.001. Epub 2018 Sep 5.

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Mitochondrial Bioenergy in Neurodegenerative Disease: Huntington and Parkinson.神经退行性疾病中的线粒体生物能量学:亨廷顿病和帕金森病。
Int J Mol Sci. 2023 Apr 13;24(8):7221. doi: 10.3390/ijms24087221.
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Neuroinflammation in Parkinson's Disease: From Gene to Clinic: A Systematic Review.
帕金森病中的神经炎症:从基因到临床:系统综述。
Int J Mol Sci. 2023 Mar 17;24(6):5792. doi: 10.3390/ijms24065792.