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通过模型揭示神经退行性疾病的分子靶点。

Unraveling Molecular Targets for Neurodegenerative Diseases Through Models.

作者信息

Xu Rongmei, Kang Qiaoju, Yang Xuefei, Yi Ping, Zhang Rongying

机构信息

School of Biotechnology and Food Engineering, Hefei University of Technology, Hefei 230002, China.

Key Laboratory of Molecular Biophysics of the Ministry of Education, College of Life Science and Technology, Huazhong University of Science and Technology, Wuhan 430074, China.

出版信息

Int J Mol Sci. 2025 Mar 26;26(7):3030. doi: 10.3390/ijms26073030.

DOI:10.3390/ijms26073030
PMID:40243699
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11988803/
Abstract

Neurodegenerative diseases (NDDs), including Alzheimer's disease (AD), Parkinson's disease (PD), amyotrophic lateral sclerosis (ALS), Huntington's disease (HD), and prion disease, represent a group of age-related disorders that pose a growing and formidable challenge to global health. Despite decades of extensive research that has uncovered key genetic factors and biochemical pathways, the precise molecular mechanisms underlying these diseases and effective therapeutic strategies remain elusive. () has emerged as a powerful model organism for studying NDDs due to its unique biological features such as genetic tractability, conserved molecular pathways, and ease of high-throughput screening. This model provides an exceptional platform for identifying molecular targets associated with NDDs and developing novel therapeutic interventions. This review highlights the critical role of in elucidating the complex molecular mechanisms of human NDDs, with a particular focus on recent advancements and its indispensable contributions to the discovery of molecular targets and therapeutic strategies for these NDDs.

摘要

神经退行性疾病(NDDs),包括阿尔茨海默病(AD)、帕金森病(PD)、肌萎缩侧索硬化症(ALS)、亨廷顿病(HD)和朊病毒病,是一组与年龄相关的疾病,对全球健康构成了日益严峻的挑战。尽管经过数十年的广泛研究,已经发现了关键的遗传因素和生化途径,但这些疾病背后的确切分子机制和有效的治疗策略仍然难以捉摸。()由于其独特的生物学特性,如遗传易处理性、保守的分子途径和易于进行高通量筛选,已成为研究神经退行性疾病的强大模式生物。该模式为识别与神经退行性疾病相关的分子靶点和开发新的治疗干预措施提供了一个特殊的平台。本综述强调了()在阐明人类神经退行性疾病复杂分子机制中的关键作用,特别关注了最近的进展及其对这些神经退行性疾病分子靶点和治疗策略发现的不可或缺的贡献。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc18/11988803/6a5ca5d9ede8/ijms-26-03030-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc18/11988803/58d707516003/ijms-26-03030-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc18/11988803/6a5ca5d9ede8/ijms-26-03030-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc18/11988803/58d707516003/ijms-26-03030-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc18/11988803/6a5ca5d9ede8/ijms-26-03030-g002.jpg

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本文引用的文献

1
Regulation of TIR-1/SARM-1 by miR-71 Protects Dopaminergic Neurons in a Model of LRRK2-Induced Parkinson's Disease.miR-71 通过调控 TIR-1/SARM-1 对 LRRK2 诱导的帕金森病模型中多巴胺能神经元起保护作用。
Int J Mol Sci. 2024 Aug 13;25(16):8795. doi: 10.3390/ijms25168795.
2
ALS-FUS mutations cause abnormal PARylation and histone H1.2 interaction, leading to pathological changes.肌萎缩侧索硬化症融合突变导致异常的 PAR 化和组蛋白 H1.2 相互作用,导致病理性改变。
Cell Rep. 2024 Aug 27;43(8):114626. doi: 10.1016/j.celrep.2024.114626. Epub 2024 Aug 19.
3
Loss of DNA glycosylases improves health and cognitive function in a C. elegans model of human tauopathy.
DNA 糖苷酶缺失可改善人类 Tau 病线虫模型的健康和认知功能。
Nucleic Acids Res. 2024 Oct 14;52(18):10965-10985. doi: 10.1093/nar/gkae705.
4
Experimental models of Parkinson's disease: Challenges and Opportunities.帕金森病的实验模型:挑战与机遇。
Eur J Pharmacol. 2024 Oct 5;980:176819. doi: 10.1016/j.ejphar.2024.176819. Epub 2024 Jul 18.
5
Polyglutamine (PolyQ) Diseases: Navigating the Landscape of Neurodegeneration.多聚谷氨酰胺(PolyQ)疾病:探索神经退行性变的全景。
ACS Chem Neurosci. 2024 Aug 7;15(15):2665-2694. doi: 10.1021/acschemneuro.4c00184. Epub 2024 Jul 12.
6
Biomarkers in Alzheimer's disease.阿尔茨海默病的生物标志物。
Clin Chim Acta. 2024 Aug 15;562:119857. doi: 10.1016/j.cca.2024.119857. Epub 2024 Jul 8.
7
Biomarkers for Managing Neurodegenerative Diseases.用于管理神经退行性疾病的生物标志物。
Biomolecules. 2024 Mar 26;14(4):398. doi: 10.3390/biom14040398.
8
Toxic gain-of-function mechanisms in ALS-FTD neurons drive autophagy and lysosome dysfunction.ALS-FTD 神经元中的毒性获得性功能机制会导致自噬和溶酶体功能障碍。
Autophagy. 2024 Sep;20(9):2102-2104. doi: 10.1080/15548627.2024.2340415. Epub 2024 Apr 18.
9
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.
10
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Dis Model Mech. 2024 Mar 1;17(3). doi: 10.1242/dmm.050473. Epub 2024 Mar 28.