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氧化性线粒体DNA损伤变体的综合性基于血液的表征意味着墨西哥裔美国人患阿尔茨海默病的代谢风险

Danielle Marie Reid¹, Robert C Barber^2,3, Harlan P Jones¹

¹Microbiology, Immunology, and Genetics, School of Biomedical Sciences, UNT Health Science Center, Fort Worth, TX, USA.

Scientific reports

|September 7, 2023

概括

线粒体DNA (mtDNA) 的氧化损伤,测量为8-oxo-guanine (8oxoG),在墨西哥裔美国人中较高,并与阿尔茨海默病 (AD) 风险相关. 这一发现突显了AD在种族差异中的潜在代谢脆弱性.

科学领域:

神经科学是一个神经科学.
遗传学遗传学是一个
生物化学生物化学

背景情况:

由于健康差异,阿尔茨海默病 (AD) 不成比例地影响弱势群体,包括西班牙裔/拉丁裔个人.
线粒体功能障碍和代谢负担可能导致AD病因学的种族差异.
8-oxo-guanine (8oxoG) 是氧化应激和线粒体功能障碍的标志物,表明线粒体DNA (mtDNA) 受损.

研究的目的:

研究血基8oxoG水平与人口,性别,2型糖尿病和AD风险在墨西哥裔美国人 (MA) 和非西班牙裔白人 (NHW) 个体之间的关联.
确定mtDNA氧化损伤是否有助于AD的种族差异.

主要方法:

分析了来自德克萨斯州阿尔茨海默氏症研究和护理联盟的MA和NHW参与者的血液样本.
测量8oxoG的水平,在两种布菲外套PBMCs和血.
评估了与人口,性别,教育,2型糖尿病和AD风险的关联.

主要成果:

与NHW相比,在MAs的buffy coat和血中观察到显著更高的8oxoG水平.
8oxoG水平与人口,性别和教育年数有显著的关联.
发现了8oxoG水平与AD风险之间的潜在关联.

结论:

墨西哥裔美国人表现出大量的mtDNA氧化损伤负担,可能导致代谢脆弱性和AD风险增加.
基于血液的8oxoG是与年龄相关的代谢功能障碍和AD病理生理学的潜在生物标志物.
解决AD的种族差异需要了解和减轻诸如氧化应激和代谢负担等因素.

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