Wallace Gregory L, Richard Emily, Peng Cynthia S, Knodt Annchen R, Hariri Ahmad R
Department of Speech, Language, and Hearing Sciences, The George Washington University, Hall of Government Room 211, 2115 G Street NW, Washington, DC, 20052, USA.
Laboratory of NeuroGenetics, Department of Psychology and Neuroscience, Duke University, Durham, NC, USA.
Brain Imaging Behav. 2020 Apr;14(2):346-352. doi: 10.1007/s11682-018-0007-x.
Behavioral traits associated with various forms of psychopathology are conceptualized as dimensional, varying from those present in a frank disorder to subclinical expression. Demonstrating links between these behavioral traits and neurobiological indicators, such as brain structure, provides one form of validation for this view. However, unlike behavioral dimensions associated with other forms of psychopathology (e.g., autism spectrum disorder, attention deficit hyperactivity disorder, antisocial disorders), eating disorder traits have not been investigated in this manner in spite of the potential that such an approach has to elucidate etiological mechanisms. Therefore, we examined for the first time neural endophenotypes of Anorexia Nervosa and Bulimia via dimensional traits (measured using the Eating Disorders Inventory-3) in a large subclinical sample of young adults (n = 456 and n = 247, respectively; ages = 18-22 years) who each provided a structural magnetic resonance imaging scan. Cortical thickness was quantified at 81,924 vertices across the cortical surface. We found: 1) increasing eating disorder traits correlated with thinner cortex in the insula and orbitofrontal cortex, among other regions, and 2) using these regions as seeds, increasing eating disorder trait scores negatively modulated structural covariance between these seed regions and other cortical regions linked to regulatory and sensorimotor functions (e.g., frontal and temporal cortices). These findings parallel those found in the clinical literature (i.e., thinner cortex in these food-related regions in individuals with eating disorders) and therefore provide evidence supporting the dimensional view of behavioral traits associated with eating disorders. Extending this approach to genetic and neuroimaging genetics studies holds promise to inform etiology.
与各种精神病理学形式相关的行为特征被概念化为维度性的,从明显疾病中存在的特征到亚临床表达不等。证明这些行为特征与神经生物学指标(如脑结构)之间的联系,为这一观点提供了一种验证形式。然而,与其他形式的精神病理学(如自闭症谱系障碍、注意力缺陷多动障碍、反社会障碍)相关的行为维度不同,尽管这种方法有阐明病因机制的潜力,但饮食失调特征尚未以这种方式进行研究。因此,我们首次在一个大型的年轻成年人亚临床样本(分别为n = 456和n = 247;年龄 = 18 - 22岁)中,通过维度特征(使用《饮食失调量表-3》测量)检查神经性厌食症和神经性贪食症的神经内表型,这些参与者均提供了结构磁共振成像扫描。在整个皮质表面的81,924个顶点处对皮质厚度进行了量化。我们发现:1)饮食失调特征增加与岛叶和眶额皮质等区域的皮质变薄相关,以及2)以这些区域为种子,饮食失调特征得分增加会对这些种子区域与其他与调节和感觉运动功能相关的皮质区域(如额叶和颞叶皮质)之间的结构协方差产生负向调节。这些发现与临床文献中的发现相似(即饮食失调个体中这些与食物相关区域的皮质较薄),因此为支持与饮食失调相关的行为特征的维度观点提供了证据。将这种方法扩展到基因和神经影像遗传学研究有望为病因学提供信息。