Berkovitch Lucie, Lee Kangjoo, Ji Jie, Helmer Markus, Rahmati Masih, Demsar Jure, Kraljic Aleksij, Matkovic Andraz, Tamayo Zailyn, Murray John, Repovs Grega, Krystal John, Martin William, Fonteneau Clara, Anticevic Alan
Department of Psychiatry, Neuroscience, and Psychology, https://ror.org/03v76x132Yale University School of Medicine, New Haven, CT, USA.
Division of Neurocognition, Neurocomputation, Neurogenetics (N3), https://ror.org/03v76x132Yale University School of Medicine, New Haven, CT, USA.
Psychol Med. 2025 Jul 4;55:e185. doi: 10.1017/S0033291725100962.
Understanding the mechanisms of major depressive disorder (MDD) improvement is a key challenge to determining effective personalized treatments.
To identify a data-driven pattern of clinical improvement in MDD and to quantify neural-to-symptom relationships according to antidepressant treatment, we performed a secondary analysis of the publicly available dataset EMBARC (Establishing Moderators and Biosignatures of Antidepressant Response in Clinical Care). In EMBARC, participants with MDD were treated either by sertraline or placebo for 8 weeks (Stage 1), and then switched to bupropion according to clinical response (Stage 2). We computed a univariate measure of clinical improvement through a principal component (PC) analysis on the variations of individual items of four clinical scales measuring depression, anxiety, suicidal ideas, and manic-like symptoms. We then investigated how initial clinical and neural factors predicted this measure during Stage 1 by running a linear model for each brain parcel's resting-state global brain connectivity (GBC) with individual improvement scores during Stage 1.
The first PC (PC1) was similar across treatment groups at stages 1 and 2, suggesting a shared pattern of symptom improvement. PC1 patients' scores significantly differed according to treatment, whereas no difference in response was evidenced between groups with the Clinical Global Impressions Scale. Baseline GBC correlated with Stage 1 PC1 scores in the sertraline but not in the placebo group.Using data-driven reduction of symptom scales, we identified a common profile of symptom improvement with distinct intensity between sertraline and placebo.
Mapping from data-driven symptom improvement onto neural circuits revealed treatment-responsive neural profiles that may aid in optimal patient selection for future trials.
了解重度抑郁症(MDD)改善的机制是确定有效的个性化治疗方法的关键挑战。
为了识别MDD临床改善的数据驱动模式,并根据抗抑郁治疗量化神经与症状的关系,我们对公开可用的数据集EMBARC(在临床护理中确定抗抑郁反应的调节因素和生物标志物)进行了二次分析。在EMBARC中,患有MDD的参与者接受舍曲林或安慰剂治疗8周(第1阶段),然后根据临床反应改用安非他酮(第2阶段)。我们通过对测量抑郁、焦虑、自杀观念和躁狂样症状的四个临床量表的各个项目的变化进行主成分(PC)分析,计算了临床改善的单变量测量值。然后,我们通过对每个脑区的静息态全脑连通性(GBC)与第1阶段的个体改善分数运行线性模型,研究了初始临床和神经因素在第1阶段如何预测这一测量值。
第1阶段和第2阶段各治疗组的第一个主成分(PC1)相似,表明存在共同的症状改善模式。PC1患者的分数因治疗而异,而临床总体印象量表在各组之间未显示出反应差异。基线GBC与舍曲林组第1阶段的PC1分数相关,但与安慰剂组无关。通过数据驱动的症状量表简化,我们确定了舍曲林和安慰剂之间具有不同强度的共同症状改善特征。
从数据驱动的症状改善映射到神经回路揭示了治疗反应性神经特征可能有助于为未来试验选择最佳患者。