Suppr超能文献

α-突触核蛋白的翻译后修饰作为帕金森病和其他突触核蛋白病的潜在生物标志物。

Alpha-synuclein post-translational modifications as potential biomarkers for Parkinson disease and other synucleinopathies.

机构信息

Proteomics Core Facility, School of Life Sciences, Station 19, Ecole Polytechnique Fédérale de Lausanne, CH-1015 Lausanne, Switzerland;

出版信息

Mol Cell Proteomics. 2013 Dec;12(12):3543-58. doi: 10.1074/mcp.R113.032730. Epub 2013 Aug 21.

Abstract

The development of novel therapies against neurodegenerative disorders requires the ability to detect their early, presymptomatic manifestations in order to enable treatment before irreversible cellular damage occurs. Precocious signs indicative of neurodegeneration include characteristic changes in certain protein levels, which can be used as diagnostic biomarkers when they can be detected in fluids such as blood plasma or cerebrospinal fluid. In the case of synucleinopathies, cerebrospinal alpha-synuclein (α-syn) has attracted great interest as a potential biomarker; however, there is ongoing debate regarding the association between cerebrospinal α-syn levels and neurodegeneration in Parkinson disease and synucleinopathies. Post-translational modifications (PTMs) have emerged as important determinants of α-syn's physiological and pathological functions. Several PTMs are enriched within Lewy bodies and exist at higher levels in α-synucleinopathy brains, suggesting that certain modified forms of α-syn might be more relevant biomarkers than the total α-syn levels. However, the quantification of PTMs in bodily fluids poses several challenges. This review describes the limitations of current immunoassay-based α-syn quantification methods and highlights how these limitations can be overcome using novel mass-spectrometry-based assays. In addition, we describe how advances in chemical synthesis, which have enabled the preparation of α-syn proteins that are site-specifically modified at single or multiple residues, can facilitate the development of more accurate assays for detecting and quantifying α-syn PTMs in health and disease.

摘要

新型神经退行性疾病治疗方法的开发需要能够检测到疾病的早期、无症状表现,以便在细胞发生不可逆转损伤之前进行治疗。神经退行性变的早期标志包括某些蛋白质水平的特征性变化,当这些变化可以在血液血浆或脑脊液等体液中检测到时,它们可以用作诊断生物标志物。在突触核蛋白病中,脑脊液α-突触核蛋白(α-syn)作为一种潜在的生物标志物引起了极大的关注;然而,脑脊液α-syn 水平与帕金森病和突触核蛋白病中的神经退行性变之间的关联仍存在争议。翻译后修饰(PTMs)已成为 α-syn 生理和病理功能的重要决定因素。几种 PTMs 在路易体中富集,并存在于突触核蛋白病大脑中的更高水平,这表明某些修饰形式的 α-syn 可能比总 α-syn 水平更相关的生物标志物。然而,在体液中定量 PTMs 存在一些挑战。本综述描述了当前基于免疫测定的 α-syn 定量方法的局限性,并强调了如何使用新型基于质谱的测定方法克服这些局限性。此外,我们描述了化学合成的进展如何使能够制备在单个或多个残基处特异性修饰的 α-syn 蛋白,从而促进开发更准确的检测和定量健康和疾病中 α-syn PTMs 的方法。

相似文献

1
Alpha-synuclein post-translational modifications as potential biomarkers for Parkinson disease and other synucleinopathies.
Mol Cell Proteomics. 2013 Dec;12(12):3543-58. doi: 10.1074/mcp.R113.032730. Epub 2013 Aug 21.
2
Phosphorylated α-synuclein as a potential biomarker for Parkinson's disease and related disorders.
Expert Rev Mol Diagn. 2012 Mar;12(2):115-7. doi: 10.1586/erm.12.5.
3
Post-translational modifications of soluble α-synuclein regulate the amplification of pathological α-synuclein.
Nat Neurosci. 2023 Feb;26(2):213-225. doi: 10.1038/s41593-022-01239-7. Epub 2023 Jan 23.
6
Cerebrospinal fluid Tau/α-synuclein ratio in Parkinson's disease and degenerative dementias.
Mov Disord. 2011 Jul;26(8):1428-35. doi: 10.1002/mds.23670. Epub 2011 Apr 5.
7
Characterization of molecular biomarkers in cerebrospinal fluid and serum of E46K-SNCA mutation carriers.
Parkinsonism Relat Disord. 2022 Mar;96:29-35. doi: 10.1016/j.parkreldis.2022.01.024. Epub 2022 Feb 5.
8
Development of a Novel Electrochemiluminescence ELISA for Quantification of α-Synuclein Phosphorylated at Ser in Biological Samples.
ACS Chem Neurosci. 2023 Apr 5;14(7):1238-1248. doi: 10.1021/acschemneuro.2c00676. Epub 2023 Mar 15.
9
Cerebrospinal fluid alpha-synuclein in neurodegenerative disorders-a marker of synapse loss?
Neurosci Lett. 2009 Feb 6;450(3):332-5. doi: 10.1016/j.neulet.2008.11.015. Epub 2008 Nov 12.

引用本文的文献

2
Differential role of C-terminal truncations on alpha-synuclein pathology and Lewy body formation.
NPJ Parkinsons Dis. 2025 Aug 26;11(1):261. doi: 10.1038/s41531-025-01084-y.
3
Phosphorylated α-synuclein in CSF and plasma does not reflect synucleinopathy.
NPJ Parkinsons Dis. 2025 Aug 7;11(1):232. doi: 10.1038/s41531-025-01086-w.
4
α-Synuclein Pathology in Synucleinopathies: Mechanisms, Biomarkers, and Therapeutic Challenges.
Int J Mol Sci. 2025 Jun 4;26(11):5405. doi: 10.3390/ijms26115405.
5
Ligands for Protein Fibrils of Amyloid-β, α-Synuclein, and Tau.
Chem Rev. 2025 Jun 11;125(11):5282-5348. doi: 10.1021/acs.chemrev.4c00838. Epub 2025 May 6.
6
Galangin reduces MPTP-induced dopamine neuron injury via the autophagy dependent-PI3K/AKT pathway.
Front Aging Neurosci. 2025 Apr 4;17:1568002. doi: 10.3389/fnagi.2025.1568002. eCollection 2025.
7
Accumulation of alpha-synuclein pathology in the liver exhibits post-translational modifications associated with Parkinson's disease.
iScience. 2024 Nov 23;27(12):111448. doi: 10.1016/j.isci.2024.111448. eCollection 2024 Dec 20.
9
Folding of N-terminally acetylated α-synuclein upon interaction with lipid membranes.
Biophys J. 2024 Nov 5;123(21):3698-3720. doi: 10.1016/j.bpj.2024.09.019. Epub 2024 Sep 21.

本文引用的文献

1
One-pot total chemical synthesis of human α-synuclein.
Chem Commun (Camb). 2013 Oct 18;49(81):9254-6. doi: 10.1039/c3cc45353g.
3
G51D α-synuclein mutation causes a novel parkinsonian-pyramidal syndrome.
Ann Neurol. 2013 Apr;73(4):459-71. doi: 10.1002/ana.23894.
4
Proteoform: a single term describing protein complexity.
Nat Methods. 2013 Mar;10(3):186-7. doi: 10.1038/nmeth.2369.
5
A novel α-synuclein missense mutation in Parkinson disease.
Neurology. 2013 Mar 12;80(11):1062-4. doi: 10.1212/WNL.0b013e31828727ba. Epub 2013 Feb 20.
6
α-Synucleinopathy associated with G51D SNCA mutation: a link between Parkinson's disease and multiple system atrophy?
Acta Neuropathol. 2013 May;125(5):753-69. doi: 10.1007/s00401-013-1096-7. Epub 2013 Feb 12.
7
Protein digestion: an overview of the available techniques and recent developments.
J Proteome Res. 2013 Mar 1;12(3):1067-77. doi: 10.1021/pr301201x. Epub 2013 Feb 15.
9
Low CSF levels of both α-synuclein and the α-synuclein cleaving enzyme neurosin in patients with synucleinopathy.
PLoS One. 2013;8(1):e53250. doi: 10.1371/journal.pone.0053250. Epub 2013 Jan 8.
10
Αlpha-synuclein levels in blood plasma from LRRK2 mutation carriers.
PLoS One. 2012;7(12):e52312. doi: 10.1371/journal.pone.0052312. Epub 2012 Dec 27.

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验