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青少年焦虑障碍与端粒长度和表观遗传年龄加速。

Telomere length and epigenetic age acceleration in adolescents with anxiety disorders.

机构信息

Anxiety Disorders Outpatient Program for Children and Adolescents, Protaia, Federal University of Rio Grande do Sul, UFRGS/Hospital de Clínicas de Porto Alegre, HCPA, Porto Alegre, Brazil.

Graduate Program in Psychiatry and Behavioral Sciences, Federal University of Rio Grande do Sul, UFRGS, Porto Alegre, Brazil.

出版信息

Sci Rep. 2021 Apr 8;11(1):7716. doi: 10.1038/s41598-021-87045-w.

Abstract

Evidence on the relationship between genetics and mental health are flourishing. However, few studies are evaluating early biomarkers that might link genes, environment, and psychopathology. We aimed to study telomere length (TL) and epigenetic age acceleration (AA) in a cohort of adolescents with and without anxiety disorders (N = 234). We evaluated a representative subsample of participants at baseline and after 5 years (n = 76) and categorized them according to their anxiety disorder diagnosis at both time points: (1) control group (no anxiety disorder, n = 18), (2) variable group (anxiety disorder in one evaluation, n = 38), and (3) persistent group (anxiety disorder at both time points, n = 20). We assessed relative mean TL by real-time quantitative PCR and DNA methylation by Infinium HumanMethylation450 BeadChip. We calculated AA using the Horvath age estimation algorithm and analyzed differences among groups using generalized linear mixed models. The persistent group of anxiety disorder did not change TL over time (p = 0.495). The variable group had higher baseline TL (p = 0.003) but no accelerated TL erosion in comparison to the non-anxiety control group (p = 0.053). Furthermore, there were no differences in AA among groups over time. Our findings suggest that adolescents with chronic anxiety did not change telomere length over time, which could be related to a delay in neuronal development in this period of life.

摘要

遗传与心理健康之间关系的证据正在不断涌现。然而,很少有研究评估可能将基因、环境和精神病理学联系起来的早期生物标志物。我们旨在研究有和没有焦虑障碍的青少年队列中的端粒长度(TL)和表观遗传年龄加速(AA)(N=234)。我们在基线和 5 年后评估了一组具有代表性的参与者样本(n=76),并根据他们在两个时间点的焦虑障碍诊断对他们进行了分类:(1)对照组(无焦虑障碍,n=18),(2)变量组(一个评估时有焦虑障碍,n=38),和(3)持续组(两个时间点都有焦虑障碍,n=20)。我们通过实时定量 PCR 评估相对平均 TL,并通过 Infinium HumanMethylation450 BeadChip 评估 DNA 甲基化。我们使用 Horvath 年龄估计算法计算 AA,并使用广义线性混合模型分析组间差异。持续存在的焦虑障碍组的 TL 随时间没有变化(p=0.495)。变量组的 TL 基线较高(p=0.003),但与非焦虑对照组相比,TL 侵蚀没有加速(p=0.053)。此外,各组的 AA 随时间没有差异。我们的研究结果表明,患有慢性焦虑症的青少年 TL 随时间没有变化,这可能与生命这个时期神经元发育延迟有关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/792e/8032711/f4011b48f7a2/41598_2021_87045_Fig1_HTML.jpg

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