Frissen Aleida, van Os Jim, Habets Petra, Gronenschild Ed, Marcelis Machteld
Department of Psychiatry and Psychology, Maastricht University, Maastricht, The Netherlands.
King's College London, King's Health Partners, Department of Psychosis Studies, Institute of Psychiatry, London, United Kingdom.
PLoS One. 2017 Jan 3;12(1):e0166651. doi: 10.1371/journal.pone.0166651. eCollection 2017.
The alterations in cortical morphology, such as cortical thinning, observed in psychotic disorder, may be the outcome of interacting genetic and environmental effects. It has been suggested that urban upbringing may represent a proxy environmental effect impacting cortical thickness (CT). Therefore, the current study examined whether the association between group as a proxy genetic variable (patients with psychotic disorder [high genetic risk], healthy siblings of patients [intermediate risk] and healthy control subjects [average risk]) and CT was conditional on different levels of the childhood urban environment and whether this was sex-dependent.
T1-weighted MRI scans were acquired from 89 patients with a psychotic disorder, 95 non-psychotic siblings of patients with psychotic disorder and 87 healthy control subjects. Freesurfer software was used to measure CT. Developmental urban exposure was classified as low, medium, and high, reflecting the population density and the number of moves between birth and the 15th birthday, using data from the Dutch Central Bureau of Statistics and the equivalent database in Belgium. Multilevel regression analyses were used to examine the association between group, sex, and urban upbringing (as well as their interactions) and cortical CT as the dependent variable.
CT was significantly smaller in the patient group compared to the controls (B = -0.043, p <0.001), but not in the siblings compared to the controls (B = -0.013, p = 0.31). There was no main effect of developmental urbanicity on CT (B = 0.001, p = 0.91). Neither the three-way group × urbanicity × sex interaction (χ2 = 3.73, p = 0.16), nor the two-way group × urbanicity interaction was significant (χ2 = 0.51, p = 0.77).
The negative association between (familial risk for) psychotic disorder and CT was not moderated by developmental urbanicity, suggesting that reduced CT is not the outcome of familial sensitivity to the proxy environmental factor 'urban upbringing'.
在精神障碍中观察到的皮质形态改变,如皮质变薄,可能是基因与环境相互作用的结果。有人提出,城市成长环境可能代表了一种影响皮质厚度(CT)的环境因素。因此,本研究调查了作为基因变量代表的组别(精神障碍患者[高遗传风险]、患者的健康兄弟姐妹[中等风险]和健康对照者[平均风险])与CT之间的关联是否取决于儿童时期不同水平的城市环境,以及这是否存在性别差异。
对89名精神障碍患者、95名精神障碍患者的非精神障碍兄弟姐妹以及87名健康对照者进行了T1加权磁共振成像扫描。使用FreeSurfer软件测量CT。利用荷兰中央统计局和比利时等效数据库的数据,将发育过程中的城市暴露分为低、中、高三个等级,反映出生至15岁之间的人口密度和搬家次数。采用多水平回归分析来研究组别、性别和城市成长环境(及其相互作用)与作为因变量的皮质CT之间的关联。
与对照组相比,患者组的CT显著更小(B = -0.043,p <0.001),但与对照组相比,兄弟姐妹组的CT没有显著差异(B = -0.013,p = 0.31)。发育过程中的城市化程度对CT没有主效应(B = 0.001,p = 0.91)。组别×城市化程度×性别三向交互作用(χ2 = 3.73,p = 0.16)以及组别×城市化程度双向交互作用均不显著(χ2 = 0.51,p = 0.77)。
精神障碍(家族风险)与CT之间的负相关不受发育过程中的城市化程度影响,这表明CT降低并非家族对“城市成长环境”这一环境因素敏感性的结果。