Scholl Jamie L, Pearson Kami, Fercho Kelene A, Van Asselt Austin J, Kallsen Noah A, Ehli Erik A, Potter Kari N, Brown-Rice Kathleen A, Forster Gina L, Baugh Lee A
Division of Basic Biomedical Sciences & Center for Brain and Behavior Research, Sanford School of Medicine, University of South Dakota, Vermillion, SD 57069, USA.
Kansas City University Center for Research, KCU, Kansas City, MO 64106, USA.
Brain Sci. 2024 Dec 16;14(12):1263. doi: 10.3390/brainsci14121263.
It is known that being the adult child of a parent with an alcohol use disorder (ACoA) can confer a wide variety of increased health and psychological risks, including higher rates of anxiety, depression, and post-traumatic stress disorder symptoms. Additionally, ACoAs are at greater risk of developing alcohol/substance use disorders (AUDs/SUDs) than individuals from families without a history of AUDs.
ACoA individuals with risky hazardous alcohol use ( = 14) and those not engaged in hazardous use ( = 14) were compared to a group of healthy controls. We examined structural brain differences and applied machine learning algorithms to predict biological brain and DNA methylation ages to investigate differences and determine any accelerated aging between these groups.
Hazardous and non-hazardous ACoA groups had lower predicted brain ages than the healthy control group ( = 100), which may result from neuro-developmental differences between ACoA groups and controls. Within specific brain regions, we observed decreased cortical volume within bilateral pars orbitalis and frontal poles, and the left middle temporal gyrus and entorhinal cortex within the hazardous alcohol ACoA group. When looking at the epigenetic aging data, the hazardous ACoA participants had increased predicted epigenetic age difference scores compared to the control group ( = 34) and the non-hazardous ACoA participant groups.
The results demonstrate a decreased brain age in the ACoAs compared to control, concurrent with increased epigenetic age specifically in the hazardous ACoA group, laying the foundation for future research to identify individuals with an increased susceptibility to developing hazardous alcohol use. Together, these results provide a better understanding of the associations between epigenetic factors, brain structure, and alcohol use disorders.
众所周知，作为患有酒精使用障碍的父母的成年子女（ACoA）会带来各种各样更高的健康和心理风险，包括焦虑、抑郁和创伤后应激障碍症状的发生率更高。此外，与没有酒精使用障碍病史的家庭中的个体相比，ACoA患酒精/物质使用障碍（AUDs/SUDs）的风险更大。
将有危险有害酒精使用行为的ACoA个体（n = 14）和未参与有害使用行为的ACoA个体（n = 14）与一组健康对照进行比较。我们检查了大脑结构差异，并应用机器学习算法来预测生物脑龄和DNA甲基化年龄，以研究这些组之间的差异并确定是否存在任何加速衰老。
危险和非危险ACoA组的预测脑龄低于健康对照组（n = 100），这可能是由于ACoA组与对照组之间的神经发育差异所致。在特定脑区，我们观察到危险酒精ACoA组双侧眶部和额极、左侧颞中回和内嗅皮质的皮质体积减小。在查看表观遗传衰老数据时，与对照组（n = 34）和非危险ACoA参与者组相比，危险ACoA参与者的预测表观遗传年龄差异得分增加。
结果表明，与对照组相比，ACoA的脑龄降低，同时特别是在危险ACoA组中表观遗传年龄增加，为未来研究确定对发展为危险酒精使用易感性增加的个体奠定了基础。总之，这些结果有助于更好地理解表观遗传因素、脑结构和酒精使用障碍之间的关联。
