• 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

无脊椎动物模型阐明帕金森病神经退行性变的机制。

Invertebrate Models Untangle the Mechanism of Neurodegeneration in Parkinson's Disease.

机构信息

Department of Neurology, University of Kansas Medical Center, Kansas City, KS 66160, USA.

出版信息

Cells. 2021 Feb 16;10(2):407. doi: 10.3390/cells10020407.

DOI:10.3390/cells10020407
PMID:33669308
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7920059/
Abstract

Parkinson's disease (PD) is the second most common neurodegenerative disease, afflicting ~10 million people worldwide. Although several genes linked to PD are currently identified, PD remains primarily an idiopathic disorder. Neuronal protein α-synuclein is a major player in disease progression of both genetic and idiopathic forms of PD. However, it cannot alone explain underlying pathological processes. Recent studies demonstrate that many other risk factors can accelerate or further worsen brain dysfunction in PD patients. Several PD models, including non-mammalian eukaryotic organisms, have been developed to identify and characterize these factors. This review discusses recent findings in three PD model organisms, i.e., yeast, Drosophila, and , that opened new mechanisms and identified novel contributors to this disorder. These non-mammalian models share many conserved molecular pathways and cellular processes with humans. New players affecting PD pathogenesis include previously unknown genes/proteins, novel signaling pathways, and low molecular weight substances. These findings might respond to the urgent need to discover novel drug targets for PD treatment and new biomarkers for early diagnostics of this disease. Since the study of neurodegeneration using simple eukaryotic organisms brought a huge amount of information, we include only the most recent or the most important relevant data.

摘要

帕金森病(PD)是第二常见的神经退行性疾病,影响全球约 1000 万人。尽管目前已经确定了几个与 PD 相关的基因,但 PD 仍然主要是一种特发性疾病。神经元蛋白α-突触核蛋白是遗传和特发性 PD 两种形式疾病进展的主要参与者。然而,它本身并不能解释潜在的病理过程。最近的研究表明,许多其他风险因素可以加速或进一步恶化 PD 患者的脑功能障碍。已经开发了几种 PD 模型,包括非哺乳动物真核生物,以鉴定和表征这些因素。本文综述了三种 PD 模式生物(酵母、果蝇和秀丽隐杆线虫)的最新发现,这些发现揭示了该疾病的新机制和新的致病因素。这些非哺乳动物模型与人类具有许多保守的分子途径和细胞过程。影响 PD 发病机制的新参与者包括以前未知的基因/蛋白质、新的信号通路和低分子量物质。这些发现可能有助于满足发现 PD 治疗新靶点和该疾病早期诊断新生物标志物的迫切需求。由于使用简单真核生物研究神经退行性变带来了大量信息,我们仅包括最近或最重要的相关数据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/db10/7920059/01a8dee66ceb/cells-10-00407-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/db10/7920059/01a8dee66ceb/cells-10-00407-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/db10/7920059/01a8dee66ceb/cells-10-00407-g001.jpg

相似文献

1
Invertebrate Models Untangle the Mechanism of Neurodegeneration in Parkinson's Disease.无脊椎动物模型阐明帕金森病神经退行性变的机制。
Cells. 2021 Feb 16;10(2):407. doi: 10.3390/cells10020407.
2
Studying Parkinson's disease using Caenorhabditis elegans models in microfluidic devices.利用微流控装置中的秀丽隐杆线虫模型研究帕金森病。
Integr Biol (Camb). 2019 May 1;11(5):186-207. doi: 10.1093/intbio/zyz017.
3
Potential Therapeutic Effects of Policosanol from Insect Wax on Caenorhabditis elegans Models of Parkinson's Disease.昆虫蜡源植物固醇对秀丽隐杆线虫帕金森病模型的潜在治疗作用。
J Neuroimmune Pharmacol. 2023 Jun;18(1-2):127-144. doi: 10.1007/s11481-022-10057-4. Epub 2023 Jan 13.
4
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.
5
Metabolic rescue of α-synuclein-induced neurodegeneration through propionate supplementation and intestine-neuron signaling in C. elegans.通过丙酸补充和线虫肠道-神经元信号传导对 α-突触核蛋白诱导的神经退行性变进行代谢挽救。
Cell Rep. 2024 Mar 26;43(3):113865. doi: 10.1016/j.celrep.2024.113865. Epub 2024 Feb 26.
6
Dysregulation of the Mitochondrial Unfolded Protein Response Induces Non-Apoptotic Dopaminergic Neurodegeneration in Models of Parkinson's Disease.线粒体未折叠蛋白反应失调在帕金森病模型中诱导非凋亡性多巴胺能神经变性。
J Neurosci. 2017 Nov 15;37(46):11085-11100. doi: 10.1523/JNEUROSCI.1294-17.2017. Epub 2017 Oct 13.
7
Anti-Parkinsonian effects of β-amyrin are regulated via LGG-1 involved autophagy pathway in Caenorhabditis elegans.β-香树脂醇通过 LGG-1 调控自噬通路对秀丽隐杆线虫帕金森样疾病的治疗作用。
Phytomedicine. 2017 Dec 1;36:118-125. doi: 10.1016/j.phymed.2017.09.002. Epub 2017 Sep 21.
8
Acetaminophen attenuates dopamine neuron degeneration in animal models of Parkinson's disease.对乙酰氨基酚可减轻帕金森病动物模型中的多巴胺能神经元变性。
Neurosci Lett. 2008 Jul 11;439(2):129-33. doi: 10.1016/j.neulet.2008.05.003. Epub 2008 May 7.
9
The prion-like spreading of α-synuclein: From in vitro to in vivo models of Parkinson's disease.α-突触核蛋白的朊病毒样传播:从帕金森病的体外到体内模型。
Ageing Res Rev. 2019 Mar;50:89-101. doi: 10.1016/j.arr.2019.01.012. Epub 2019 Jan 25.
10
Rescuing defective vesicular trafficking protects against alpha-synuclein toxicity in cellular and animal models of Parkinson's disease.在帕金森病的细胞和动物模型中,挽救有缺陷的囊泡运输可抵御α-突触核蛋白毒性。
ACS Chem Biol. 2006 Aug 22;1(7):420-4. doi: 10.1021/cb600331e.

引用本文的文献

1
Parkinson's Disease: Bridging Gaps, Building Biomarkers, and Reimagining Clinical Translation.帕金森病:弥合差距、构建生物标志物及重塑临床转化
Cells. 2025 Jul 28;14(15):1161. doi: 10.3390/cells14151161.
2
Research models to study lewy body dementia.用于研究路易体痴呆的研究模型。
Mol Neurodegener. 2025 Apr 23;20(1):46. doi: 10.1186/s13024-025-00837-w.
3
Bridging the gap: investigating the role of phosphorylation at the serine 129 site of α-synuclein in VAPB-PTPIP51 interactions.弥合差距:研究α-突触核蛋白丝氨酸129位点磷酸化在VAPB-PTPIP51相互作用中的作用。

本文引用的文献

1
Doxycycline inhibits α-synuclein-associated pathologies in vitro and in vivo.强力霉素抑制α-突触核蛋白相关的体内外病变。
Neurobiol Dis. 2021 Apr;151:105256. doi: 10.1016/j.nbd.2021.105256. Epub 2021 Jan 8.
2
Observation of an α-synuclein liquid droplet state and its maturation into Lewy body-like assemblies.观察到α-突触核蛋白的液滴状态及其成熟为路易体样聚集体。
J Mol Cell Biol. 2021 Aug 4;13(4):282-294. doi: 10.1093/jmcb/mjaa075.
3
Comparative proteomic analysis highlights metabolic dysfunction in α-synucleinopathy.比较蛋白质组学分析突出了α-突触核蛋白病中的代谢功能障碍。
Acta Neuropathol Commun. 2025 Feb 24;13(1):40. doi: 10.1186/s40478-025-01949-6.
4
Blood-brain barrier alterations and their impact on Parkinson's disease pathogenesis and therapy.血脑屏障改变及其对帕金森病发病机制和治疗的影响。
Transl Neurodegener. 2024 Jul 29;13(1):37. doi: 10.1186/s40035-024-00430-z.
5
Flight to insight: maximizing the potential of models of C9orf72-FTD.洞察之旅:最大化C9orf72型额颞叶痴呆模型的潜力
Front Mol Neurosci. 2024 Jun 10;17:1434443. doi: 10.3389/fnmol.2024.1434443. eCollection 2024.
6
Rotenone-induced PINK1/Parkin-mediated mitophagy: establishing a silkworm model for Parkinson's disease potential.鱼藤酮诱导的PINK1/Parkin介导的线粒体自噬:建立帕金森病潜在的家蚕模型。
Front Mol Neurosci. 2024 Apr 19;17:1359294. doi: 10.3389/fnmol.2024.1359294. eCollection 2024.
7
Invertebrate genetic models of amyotrophic lateral sclerosis.肌萎缩侧索硬化症的无脊椎动物遗传模型。
Front Mol Neurosci. 2024 Mar 4;17:1328578. doi: 10.3389/fnmol.2024.1328578. eCollection 2024.
8
Exploring Caenorhabditis elegans as Parkinson's Disease Model: Neurotoxins and Genetic Implications.探索秀丽隐杆线虫作为帕金森病模型:神经毒素和遗传影响。
Neurotox Res. 2024 Feb 6;42(1):11. doi: 10.1007/s12640-024-00686-3.
9
Chiisanoside Mediates the Parkin/ZNF746/PGC-1α Axis by Downregulating MiR-181a to Improve Mitochondrial Biogenesis in 6-OHDA-Caused Neurotoxicity Models In Vitro and In Vivo: Suggestions for Prevention of Parkinson's Disease.赤芝糖苷通过下调miR-181a介导Parkin/ZNF746/PGC-1α轴,以改善6-OHDA诱导的体外和体内神经毒性模型中的线粒体生物发生:对帕金森病预防的建议
Antioxidants (Basel). 2023 Sep 20;12(9):1782. doi: 10.3390/antiox12091782.
10
Assessing Curcumin Uptake and Clearance and Their Influence on Superoxide Dismutase Activity in .评估姜黄素的摄取与清除及其对超氧化物歧化酶活性的影响 。(原文结尾不完整,推测可能是在某个特定环境或细胞等中的相关研究,但仅依据现有内容只能这样翻译)
BioTech (Basel). 2023 Sep 8;12(3):58. doi: 10.3390/biotech12030058.
NPJ Parkinsons Dis. 2020 Dec 11;6(1):40. doi: 10.1038/s41531-020-00143-w.
4
Myosin V-mediated transport of Snc1 and Vps10 toward the trans-Golgi network.肌球蛋白 V 介导的 Snc1 和 Vps10 向反式高尔基网络的运输。
Eur J Cell Biol. 2021 Apr;100(3):151143. doi: 10.1016/j.ejcb.2020.151143. Epub 2020 Nov 30.
5
ATP13A2-mediated endo-lysosomal polyamine export counters mitochondrial oxidative stress.ATP13A2 介导的内溶酶体多胺输出可抵抗线粒体氧化应激。
Proc Natl Acad Sci U S A. 2020 Dec 8;117(49):31198-31207. doi: 10.1073/pnas.1922342117. Epub 2020 Nov 23.
6
Spen modulates lipid droplet content in adult Drosophila glial cells and protects against paraquat toxicity.Spen 调节成年果蝇神经胶质细胞中的脂滴含量并抵御百草枯毒性。
Sci Rep. 2020 Nov 18;10(1):20023. doi: 10.1038/s41598-020-76891-9.
7
Ring Finger Protein 11 (RNF11) Modulates Dopamine Release in Drosophila.无名指蛋白11(RNF11)调节果蝇中的多巴胺释放。
Neuroscience. 2021 Jan 1;452:37-48. doi: 10.1016/j.neuroscience.2020.10.021. Epub 2020 Nov 8.
8
Epigenetic Changes and Its Intervention in Age-Related Neurodegenerative Diseases.表观遗传变化及其对年龄相关性神经退行性疾病的干预
Cell Mol Neurobiol. 2022 Apr;42(3):577-595. doi: 10.1007/s10571-020-00979-z. Epub 2020 Oct 19.
9
Robust Sequence Determinants of α-Synuclein Toxicity in Yeast Implicate Membrane Binding.α-突触核蛋白毒性在酵母中的稳健序列决定因素暗示了其与膜的结合。
ACS Chem Biol. 2020 Aug 21;15(8):2137-2153. doi: 10.1021/acschembio.0c00339. Epub 2020 Aug 12.
10
TDP-1/TDP-43 potentiates human α-Synuclein (HASN) neurodegeneration in Caenorhabditis elegans.TDP-1/TDP-43 增强人类 α-突触核蛋白(HASN)在秀丽隐杆线虫中的神经退行性变。
Biochim Biophys Acta Mol Basis Dis. 2020 Oct 1;1866(10):165876. doi: 10.1016/j.bbadis.2020.165876. Epub 2020 Jun 9.