Reduced Cortical Thickness as an Outcome of Differential Sensitivity to Environmental Risks in Schizophrenia
Reduced Cortical Thickness as an Outcome of Differential Sensitivity to Environmental Risks in Schizophrenia
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DOI：
10.1016/j.biopsych.2010.08.010
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发表时间：
2011-03-01
影响因子：
10.6
通讯作者：
van Os, Jim
中科院分区：
文献类型：
--
作者：
Habets, Petra;Marcelis, Machteld;van Os, Jim
背景：精神分裂症的病因学被认为涉及对环境暴露的不同可能的遗传介导的敏感性。然而，精神病理学结构的模型中的差异敏感性的检查受到偏见，因为精神病理学本身可能会扭曲暴露评估。相反，神经影像表型的使用可能为环境暴露的差异敏感性提供无偏倚的证据。本研究探讨了两个环境暴露与精神分裂症和磁共振成像（MRI）大脑皮层thickness.Methods模型的大脑改变的影响：T1加权MRI扫描获得88例精神分裂症患者，98名健康的同胞高于平均遗传风险的精神分裂症，和87名对照组。使用Freesurfer软件测量68个脑区的皮质厚度。1）皮质厚度和2）大麻使用和发育创伤之间的关联进行了检查。显著的X组发育创伤相互作用（chi（2）= 9.65，p = 0.01）以及显著的X组大麻相互作用（chi（2）= 6.04，p = 0.05）是明显的，表明患者组的敏感性不同，这两种暴露都显示出皮质厚度的更强的减少。在大麻的同胞对照比较中发现了类似的模式。对于发育性创伤，兄弟姐妹没有不同的对照组，显示皮质厚度增加，更高水平的traumatic.Conclusions：研究结果表明，精神分裂症及其遗传易感性与差异大脑皮层的敏感性，如大麻的发展环境暴露。基因-环境相互作用可能是精神分裂症患者及其亲属中观察到的一些大脑改变的基础。
Background: The etiology of schizophrenia is thought to involve differential likely genetically mediated sensitivity to environmental exposures. However, examination of differential sensitivity in models of psychopathologic constructs is subject to bias because psychopathology itself may distort exposure assessment. The use of neuroimaging phenotypes, conversely, may provide unbiased evidence for differential sensitivity to environmental exposures. This study examined the impact of two environmental exposures associated with both schizophrenia and magnetic resonance imaging (MRI) cerebral alterations in models of cerebral cortical thickness.Methods: T1-weighted MRI scans were acquired from 88 patients with schizophrenia, 98 healthy siblings at higher than average genetic risk for schizophrenia, and 87 control subjects. Freesurfer software was used to measure cortical thickness for 68 brain regions. Associations between 1) cortical thickness and 2) cannabis use and developmental trauma were examined.Results: A significant group X developmental trauma interaction (chi(2) = 9.65, p = .01), as well as a significant group x cannabis interaction (chi(2) = 6.04, p = .05) was apparent, indicating differential sensitivity of the patient group, which displayed stronger reductions of cortical thickness for both exposures. A similar pattern was found in the sibling-control comparison for cannabis. For developmental trauma, siblings did not differ from control subjects, displaying an increase in cortical thickness with higher levels of trauma.Conclusions: The findings suggest that schizophrenia and its genetic liability are associated with differential cerebral cortical sensitivity to developmental environmental exposures such as cannabis. Gene-environment interactions may underlie some of the brain alterations observed in patients with schizophrenia and their relatives.