Kumar Kuldeep, Liao Zhijie, Kopal Jakub, Moreau Clara, Ching Christopher R K, Modenato Claudia, Snyder Will, Kazem Sayeh, Martin Charles-Olivier, Bélanger Anne-Marie, Fontaine Valérie K, Jizi Khadije, Boen Rune, Huguet Guillaume, Saci Zohra, Kushan Leila, Silva Ana I, van den Bree Marianne B M, Linden David E J, Owen Michael J, Hall Jeremy, Lippé Sarah, Dumas Guillaume, Draganski Bogdan, Almasy Laura, Thomopoulos Sophia I, Jahanshad Neda, Sønderby Ida E, Andreassen Ole A, Glahn David C, Raznahan Armin, Bearden Carrie E, Paus Tomas, Thompson Paul M, Jacquemont Sébastien
Centre de recherche CHU Sainte-Justine and University of Montreal, Canada.
Centre for Precision Psychiatry, Division of Mental Health and Addiction, Institute of Clinical Medicine, University of Oslo, Oslo, Norway.
medRxiv. 2025 Apr 19:2025.04.16.25325971. doi: 10.1101/2025.04.16.25325971.
Genetic studies have identified common and rare variants increasing the risk for neurodevelopmental and psychiatric disorders (NPDs). These risk variants have also been shown to influence the structure of the cerebral cortex. However, it is unknown whether cortical differences associated with genetic variants are linked to the risk they confer for NPDs. To answer this question, we analyzed cortical thickness (CT) and surface area (SA) for common and rare variants associated with NPDs, in ~33000 individuals from the general population and clinical cohorts, as well as ENIGMA summary statistics for 8 NPDs. Rare and common genetic variants increasing risk for NPDs were preferentially associated with total SA, while NPDs were preferentially associated with mean CT. Larger effects on mean CT, but not total SA, were observed in NPD medicated subgroups. At the regional level, genetic variants were preferentially associated with effects in sensorimotor areas, while NPDs showed higher effects in association areas. We show that schizophrenia- and bipolar-disorder-associated SNPs show positive and negative effect sizes on SA suggesting that their aggregated effects cancel out in additive polygenic models. Overall, CT and SA differences associated with NPDs do not relate to those observed across individual genetic variants and may be linked with critical non-genetic factors, such as medication and the lived experience of the disorder.
基因研究已经确定了增加神经发育和精神疾病(NPDs)风险的常见和罕见变异。这些风险变异也已被证明会影响大脑皮层的结构。然而,与基因变异相关的皮层差异是否与它们赋予NPDs的风险相关尚不清楚。为了回答这个问题,我们分析了来自普通人群和临床队列的约33000名个体中与NPDs相关的常见和罕见变异的皮层厚度(CT)和表面积(SA),以及8种NPDs的ENIGMA汇总统计数据。增加NPDs风险的罕见和常见基因变异优先与总SA相关,而NPDs优先与平均CT相关。在接受药物治疗的NPD亚组中,观察到对平均CT有更大影响,但对总SA没有影响。在区域水平上,基因变异优先与感觉运动区域的效应相关,而NPDs在联合区域表现出更高的效应。我们表明,与精神分裂症和双相情感障碍相关的单核苷酸多态性(SNPs)对SA显示出正向和负向效应大小,这表明它们在加性多基因模型中的综合效应相互抵消。总体而言,与NPDs相关的CT和SA差异与个体基因变异中观察到的差异无关,可能与关键的非遗传因素有关,如药物治疗和疾病的生活经历。