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阿尔茨海默病中的循环游离DNA与DNA双链断裂

Circulating Cell Free DNA and DNA Double-Strand Breakage in Alzheimer's Disease.

作者信息

Nguyen Michelle, Wood Colby, Rios Andres, Salter Zach, Reddy P Hemachandra

机构信息

Department of Internal Medicine, Texas Tech University Health Sciences Center, Lubbock, TX, USA.

Nutritional Sciences Department, College Human Sciences, Texas Tech University, Lubbock, TX, USA.

出版信息

J Alzheimers Dis Rep. 2024 Apr 8;8(1):627-635. doi: 10.3233/ADR-240012. eCollection 2024.

Abstract

Alzheimer's disease (AD) is an age-related neurodegenerative disease that is characterized by memory loss and multiple cognitive impairments. AD is pathologically characterized by age-dependent accumulation of amyloid-β protein and the phosphorylation of tau protein in the brains of patients with AD. Clinically, manifestations of AD include cognitive decline, dementia, alterations of high-order brain functions, and movement disorders. Double-stranded DNA breaks are a lethal form of DNA damage and are typically repaired via non-homologous end joining and homologous recombination. However, in AD brain, repair mechanism is disrupted, leading to a cascade of events, cognitive dysfunction, organ failure and reduced lifespan. Increased circulating cell-free DNA in the blood, cerebrospinal fluid, and urine in patients with AD, can be used as early detectable biomarkers for AD. The purpose of our article is to explore the potential uses of cell-free DNA and double-stranded DNA breaks as prognostic markers for AD and examine the recent research on the application of these markers in studies.

摘要

阿尔茨海默病(AD)是一种与年龄相关的神经退行性疾病,其特征为记忆力丧失和多种认知障碍。AD的病理特征是AD患者大脑中β淀粉样蛋白的年龄依赖性积累和tau蛋白的磷酸化。临床上,AD的表现包括认知能力下降、痴呆、高级脑功能改变和运动障碍。双链DNA断裂是一种致命的DNA损伤形式,通常通过非同源末端连接和同源重组进行修复。然而,在AD大脑中,修复机制受到破坏,导致一系列事件、认知功能障碍、器官衰竭和寿命缩短。AD患者血液、脑脊液和尿液中循环游离DNA的增加可用作AD的早期可检测生物标志物。我们文章的目的是探讨游离DNA和双链DNA断裂作为AD预后标志物的潜在用途,并研究这些标志物在相关研究中的应用的最新进展。

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本文引用的文献

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Detection of neuron-derived cfDNA in blood plasma: a new diagnostic approach for neurodegenerative conditions.
Front Neurol. 2023 Oct 31;14:1272960. doi: 10.3389/fneur.2023.1272960. eCollection 2023.
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