Epigenetic age acceleration as a biomarker for impaired cognitive abilities in adulthood following early life adversity and psychiatric disorders

IF 4.3 2区医学 Q1 NEUROSCIENCES

Neurobiology of Stress Pub Date : 2023-10-15 DOI:10.1016/j.ynstr.2023.100577

John M. Felt , Natan Yusupov , Karra D. Harrington , Julia Fietz , Zhenyu “Zach” Zhang , Martin J. Sliwinski , Nilam Ram , Kieran J. O'Donnell , BeCOME Working Group , Michael J. Meaney , Frank W. Putnam , Jennie G. Noll , Elisabeth B. Binder , Chad E. Shenk

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引用次数: 0

Abstract

Background

Early life adversity and psychiatric disorders are associated with earlier declines in neurocognitive abilities during adulthood. These declines may be preceded by changes in biological aging, specifically epigenetic age acceleration, providing an opportunity to uncover genome-wide biomarkers that identify individuals most likely to benefit from early screening and prevention.

Methods

Five unique epigenetic age acceleration clocks derived from peripheral blood were examined in relation to latent variables of general and speeded cognitive abilities across two independent cohorts: 1) the Female Growth and Development Study (FGDS; n = 86), a 30-year prospective cohort study of substantiated child sexual abuse and non-abused controls, and 2) the Biological Classification of Mental Disorders study (BeCOME; n = 313), an adult community cohort established based on psychiatric disorders.

Results

A faster pace of biological aging (DunedinPoAm) was associated with lower general cognitive abilities in both cohorts and slower speeded abilities in the BeCOME cohort. Acceleration in the Horvath clock was significantly associated with slower speeded abilities in the BeCOME cohort but not the FGDS. Acceleration in the Hannum clock and the GrimAge clock were not significantly associated with either cognitive ability. Accelerated PhenoAge was associated with slower speeded abilities in the FGDS but not the BeCOME cohort.

Conclusions

The present results suggest that epigenetic age acceleration has the potential to serve as a biomarker for neurocognitive decline in adults with a history of early life adversity or psychiatric disorders. Estimates of epigenetic aging may identify adults at risk of cognitive decline that could benefit from early neurocognitive screening.

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表观遗传年龄加速作为成年早期生活逆境和精神障碍后认知能力受损的生物标志物

背景早期生活中的逆境和精神障碍与成年期神经认知能力的早期下降有关。在这些下降之前，生物衰老可能会发生变化，特别是表观遗传学年龄加速，这为揭示全基因组生物标志物提供了机会，这些生物标志物可以识别最有可能从早期筛查和预防中受益的个体。方法在两个独立的队列中，检测了来自外周血的五个独特的表观遗传学年龄加速时钟与一般和加速认知能力的潜在变量的关系：1）女性生长发育研究（FGDS；n=86），这是一项为期30年的前瞻性队列研究，对证实的儿童性虐待和非虐待对照进行研究，和2）精神障碍生物学分类研究（BeCOME；n=313），一个基于精神障碍建立的成人社区队列。结果生物衰老速度较快（DunedinPoAm）与两个队列中较低的一般认知能力和BeCOME队列中较慢的加速能力有关。Horvath时钟的加速与BeCOME队列中较慢的加速能力显著相关，但与FGDS无关。Hannum时钟和GrimAge时钟的加速与这两种认知能力都没有显著关联。在FGDS中，加速表型年龄与较慢的加速能力有关，但在BeCOME队列中则不然。结论目前的研究结果表明，表观遗传年龄加速有可能成为有早期生活逆境或精神障碍史的成年人神经认知能力下降的生物标志物。表观遗传学衰老的估计可能会识别出有认知能力下降风险的成年人，这可能受益于早期神经认知筛查。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Neurobiology of Stress Biochemistry, Genetics and Molecular Biology-Biochemistry

CiteScore

9.40

自引率

4.00%

发文量

审稿时长

48 days

期刊介绍： Neurobiology of Stress is a multidisciplinary journal for the publication of original research and review articles on basic, translational and clinical research into stress and related disorders. It will focus on the impact of stress on the brain from cellular to behavioral functions and stress-related neuropsychiatric disorders (such as depression, trauma and anxiety). The translation of basic research findings into real-world applications will be a key aim of the journal. Basic, translational and clinical research on the following topics as they relate to stress will be covered: Molecular substrates and cell signaling, Genetics and epigenetics, Stress circuitry, Structural and physiological plasticity, Developmental Aspects, Laboratory models of stress, Neuroinflammation and pathology, Memory and Cognition, Motivational Processes, Fear and Anxiety, Stress-related neuropsychiatric disorders (including depression, PTSD, substance abuse), Neuropsychopharmacology.