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血液 COASY DNA 甲基化水平升高可能成为阿尔茨海默病早期病理的生物标志物。

Increased blood COASY DNA methylation levels a potential biomarker for early pathology of Alzheimer's disease.

机构信息

Department of Virology, The Jikei University School of Medicine, Tokyo, Japan.

Department of Psychiatry, The Jikei University School of Medicine, Tokyo, Japan.

出版信息

Sci Rep. 2020 Jul 22;10(1):12217. doi: 10.1038/s41598-020-69248-9.

DOI:10.1038/s41598-020-69248-9
PMID:32699290
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7376092/
Abstract

Early diagnosis of dementia including Alzheimer's disease (AD) is an urgent medical and welfare issue. However, to date, no simple biometrics have been available. We reported that blood DNA methylation levels of the COASY gene, which encodes coenzyme A synthase, were increased in individuals with AD and amnestic mild cognitive impairment (aMCI). The present study sought to replicate these findings with larger numbers of samples. Another objective was to clarify whether COASY methylation is associated with neurodegeneration through a comparison of AD, AD with cardiovascular disease (CVD), and vascular dementia (VaD). We measured blood COASY methylation levels in normal controls (NCs) (n = 200), and individuals with aMCI (n = 22), AD (n = 151), and VaD (n = 21). Compared with NCs, they were significantly higher in individuals with aMCI and AD. Further, they were significantly higher in AD patients without cardiovascular diseases compared to AD patients with them. These findings suggest that COASY methylation levels may be related to neurodegeneration in AD.

摘要

早期诊断包括阿尔茨海默病(AD)在内的痴呆症是一个紧迫的医学和福利问题。然而,迄今为止,还没有简单的生物标志物可用。我们报告称,编码辅酶 A 合酶的 COASY 基因的血液 DNA 甲基化水平在 AD 和遗忘型轻度认知障碍(aMCI)患者中升高。本研究旨在用更多的样本复制这些发现。另一个目的是通过比较 AD、AD 合并心血管疾病(CVD)和血管性痴呆(VaD)来阐明 COASY 甲基化是否与神经退行性变有关。我们测量了正常对照组(NC)(n=200)、aMCI 患者(n=22)、AD 患者(n=151)和 VaD 患者(n=21)的血液 COASY 甲基化水平。与 NC 相比,aMCI 和 AD 患者的 COASY 甲基化水平显著升高。此外,与有心血管疾病的 AD 患者相比,无心血管疾病的 AD 患者的 COASY 甲基化水平显著升高。这些发现表明,COASY 甲基化水平可能与 AD 中的神经退行性变有关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/daff/7376092/afde6ba2c167/41598_2020_69248_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/daff/7376092/abb1428308f6/41598_2020_69248_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/daff/7376092/02a1977e864a/41598_2020_69248_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/daff/7376092/725ec5f6388b/41598_2020_69248_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/daff/7376092/8689139cda57/41598_2020_69248_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/daff/7376092/afde6ba2c167/41598_2020_69248_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/daff/7376092/abb1428308f6/41598_2020_69248_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/daff/7376092/02a1977e864a/41598_2020_69248_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/daff/7376092/725ec5f6388b/41598_2020_69248_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/daff/7376092/8689139cda57/41598_2020_69248_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/daff/7376092/afde6ba2c167/41598_2020_69248_Fig5_HTML.jpg

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1
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2
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J Alzheimers Dis. 2019;67(1):35-60. doi: 10.3233/JAD-180213.
3
CoA synthase regulates mitotic fidelity via CBP-mediated acetylation.辅酶 A 合酶通过 CBP 介导的乙酰化作用调节有丝分裂保真度。
Genes (Basel). 2024 Nov 25;15(12):1509. doi: 10.3390/genes15121509.
4
Blood DNA Methylation Signature for Incident Dementia: Evidence from Longitudinal Cohorts.新发痴呆症的血液DNA甲基化特征:来自纵向队列的证据。
medRxiv. 2024 Nov 26:2024.11.03.24316667. doi: 10.1101/2024.11.03.24316667.
5
MIAMI-AD (Methylation in Aging and Methylation in AD): an integrative knowledgebase that facilitates explorations of DNA methylation across sex, aging, and Alzheimer's disease.迈阿密-AD(衰老中的甲基化和 AD 中的甲基化):一个综合知识库,便于跨性别、衰老和阿尔茨海默病探索 DNA 甲基化。
Database (Oxford). 2024 Jul 19;2024. doi: 10.1093/database/baae061.
6
APOE 5'UTR Methylation Pattern Analysis in Blood and Brain Tissue from Alzheimer's Disease Affected Patients.阿尔茨海默病患者血液和脑组织中APOE 5'非翻译区甲基化模式分析
Aging Dis. 2024 Jun 24;16(3):1639-1651. doi: 10.14336/AD.2024.0350.
7
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8
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9
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10
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Nat Commun. 2018 Mar 12;9(1):1039. doi: 10.1038/s41467-018-03422-6.
4
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Methods Mol Biol. 2018;1708:551-571. doi: 10.1007/978-1-4939-7481-8_28.
5
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PLoS One. 2016 Dec 19;11(12):e0168816. doi: 10.1371/journal.pone.0168816. eCollection 2016.
6
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7
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8
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PLoS One. 2016 Jan 7;11(1):e0146449. doi: 10.1371/journal.pone.0146449. eCollection 2016.
9
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Lancet. 2015 Oct 24;386(10004):1698-706. doi: 10.1016/S0140-6736(15)00463-8.
10
Exome sequence reveals mutations in CoA synthase as a cause of neurodegeneration with brain iron accumulation.外显子组序列揭示 CoA 合酶突变是脑铁蓄积性神经退行性变的原因。
Am J Hum Genet. 2014 Jan 2;94(1):11-22. doi: 10.1016/j.ajhg.2013.11.008. Epub 2013 Dec 19.