Increased Levels of Circulating Cell-Free mtDNA in the Plasma of Subjects With Late-Life Depression and Frailty: A Preliminary Study.

Increased Levels of Circulating Cell-Free mtDNA in the Plasma of Subjects With Late-Life Depression and Frailty: A Preliminary Study.
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在患有晚期抑郁症和脆弱的受试者血浆中无细胞的循环mtDNA水平增加:一项初步研究。

DOI:
10.1016/j.jagp.2021.07.012
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发表时间:
2022-03
期刊:
The American journal of geriatric psychiatry : official journal of the American Association for Geriatric Psychiatry
影响因子:
--
通讯作者:
Diniz BS
Diniz BS
中科院分区:
其他
文献类型:
--
作者:
Ampo E;Mendes-Silva AP;Goncalves V;Bartley JM;Kuchel GA;Diniz BS

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评估循环无细胞线粒体DNA(ccf-mtDNA)水平,细胞应激和损伤的标志物,在老年抑郁症(LLD)和虚弱的老年人。我们假设,与单独的个体相比,同时患有虚弱和LLD的个体将具有更高的ccf-mtDNA水平。53名老年人(从未抑郁+健壮(参考组,n=16),LLD+健壮(n=9),从未抑郁+虚弱前期/虚弱(n=5),LLD+虚弱前期/虚弱(n=23))被纳入研究。从EDTA血浆样品中提取DNA,并通过RT-PCR定量ccf-mtDNA。我们发现各组之间的ccf-mtDNA水平存在统计学显著差异(F(3,49)=3.07,p=0.036),LLD+Pre-Frail/Frail组的个体显示出最高水平的ccf-mtDNA。LLD和虚弱的共存与细胞损伤和应激的标记物增加有关(即,ccf-mtDNA)。我们的研究结果表明,这些条件可能共享细胞应激和线粒体功能障碍现象作为一种常见的生物学机制,为这些条件的老年科学指导的干预提供了潜在的未来机会。
To evaluate the circulating cell-free mitochondrial DNA (ccf-mtDNA) levels, a marker of cellular stress and damage, in older adults with late-life depression (LLD) and frailty. We hypothesize that individuals with both frailty and LLD will have higher ccf-mtDNA levels than individuals with either condition in isolation. Fifty-three older adults (Never Depressed+Robust (reference group, n=16), LLD+Robust (n=9), Never Depressed+Pre-frail/Frail (n=5), LLD+Pre-frail/Frail (n=23)) were included in the study. DNA was extracted from EDTA plasma samples, and ccf-mtDNA was quantified by RT-PCR. We found a statistically significant difference in the levels of ccf-mtDNA across groups (F(3,49)=3.07, p=0.036), with individuals in the LLD+Pre-Frail/Frail group showing the highest levels of ccf-mtDNA. The co-existence of LLD and frailty is associated with increased markers of cellular damage and stress (i.e., ccf-mtDNA). Our results suggest that these conditions may share cellular stress and mitochondrial dysfunction phenomena as a common biological mechanism, offering potential future opportunities for geroscience-guided interventions for these conditions.
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