medRxiv : the preprint server for health sciences · 2025
Cortical differences across psychiatric disorders and associated common and rare genetic variants.
СтатьяПрепринтНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
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, 16p11.2 European Consortium, Simons Searchlight Consortium, 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
Аннотация
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.