沟深度和遗传易感性影响成人注意力缺陷/多动障碍的初始治疗反应。

IF 4.8
Jonathan Laatsch, Friederike S David, Frederike Stein, Carlo Maj, Andreas J Forstner, Simon Maier, Swantje Matthies, Esther Sobanski, Barbara Alm, Ludger Tebartz van Elst, Axel Krug, Alexandra Philipsen
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引用次数: 0

摘要

背景:随着神经生物学标志物在指导个性化治疗方面的地位日益突出,神经沟深度(SD)在神经处理和治疗效果中仍是一个未被充分探索的关键因素。虽然遗传影响着皮质结构,但它们在调节SD和治疗结果之间的关系中的作用尚不清楚。本研究探讨了治疗前SD是否能预测成人注意缺陷多动障碍(ADHD)的症状缓解,并探讨了ADHD遗传易感性和交叉障碍影响的调节作用。方法:利用来自成人ADHD研究中哌醋甲酯和心理治疗比较的结构神经影像学数据,我们研究了在为期12周的干预后,包括团体心理治疗或哌醋甲酯或安慰剂的临床管理,SD和治疗反应之间的关系。治疗前SD来自119个t1加权解剖扫描,并使用线性回归模型分析其对治疗后症状严重程度的预测价值。随后,我们探讨了多基因评分对ADHD和交叉障碍易感性的调节作用。结构分析采用计算解剖学工具箱中的无阈值聚类增强方法进行,并在SPSS(30.0.0)中进行适度分析。结果:结果显示,顶叶、颞叶和枕叶区域的SD显著预测症状缓解,将沟深与治疗效果联系起来。此外,ADHD的遗传易感性和交叉障碍特征影响了这些关系,强调了皮质结构和遗传易感性在决定治疗结果方面的相互作用。结论:这些发现强调了ADHD治疗反应的神经生物学标志物的潜力,并强调了将神经生物学和遗传因素整合到精神病学治疗效果预测模型中的重要性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Sulcal Depth and Genetic Susceptibility influence initial Treatment Response in Adults with Attention-Deficit/Hyperactivity Disorder.

Background: As neurobiological markers gain prominence in guiding personalised treatments, sulcal depth (SD) remains an underexplored yet pivotal factor in neural processing and therapeutic efficacy. While genetic influences shape cortical architecture, their role in modulating the relationship between SD and treatment outcomes remain unclear. This study investigates whether pre-treatment SD predicts symptom alleviation in adults with Attention-Deficit/Hyperactivity Disorder (ADHD) and explores moderating effects of genetic susceptibility for ADHD and cross-disorder influences.

Methods: Using structural neuroimaging data from the Comparison of Methylphenidate and Psychotherapy in Adult ADHD Study, we examined associations between SD and treatment response following a 12-week intervention involving either group psychotherapy or clinical management with methylphenidate or placebo. Pre-treatment SD was derived from 119 T1-weighted anatomical scans and analysed using linear regression models to assess its predictive value for post-treatment symptom severity. Subsequently, we explored the moderating role of polygenic scores for ADHD and cross-disorder susceptibility. Structural analyses were performed using the threshold-free cluster enhancement approach in the Computational Anatomy Toolbox, with moderation analyses conducted in SPSS (30.0.0).

Results: Results revealed that SD in parietal, temporal, and occipital regions significantly predicted symptom alleviation, linking deeper sulci with greater treatment efficacy. Moreover, genetic predisposition for ADHD and cross-disorder traits influenced these relationships, highlighting an interaction between cortical structure and genetic susceptibility in determining treatment outcomes.

Conclusion: These findings highlight SD as a promising neurobiological marker of ADHD treatment response and emphasize the importance of integrating neurobiological- and genetic factors into predictive models of therapeutic efficacy in psychiatry.

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