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Brain multimodal co-alterations related to delay discounting: a multimodal MRI fusion analysis in persons with and without cocaine use disorder

机译:脑多模式共同改变与延迟折扣有关:具有和不含可卡因使用障碍的人的多峰MRI融合分析

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Delay discounting has been proposed as a behavioral marker of substance use disorders. Innovative analytic approaches that integrate information from multiple neuroimaging modalities can provide new insights into the complex effects of drug use on the brain. This study implemented a supervised multimodal fusion approach to reveal neural networks associated with delay discounting that distinguish persons with and without cocaine use disorder (CUD). Adults with (n?=?35) and without (n?=?37) CUD completed a magnetic resonance imaging (MRI) scan to acquire high-resolution anatomical, resting-state functional, and diffusion-weighted images. Pre-computed features from each data modality included whole-brain voxel-wise maps for gray matter volume, fractional anisotropy, and regional homogeneity, respectively. With delay discounting as the reference, multimodal canonical component analysis plus joint independent component analysis was used to identify co-alterations in brain structure and function. The sample was 58% male and 78% African–American. As expected, participants with CUD had higher delay discounting compared to those without CUD. One joint component was identified that correlated with delay discounting across all modalities, involving regions in the thalamus, dorsal striatum, frontopolar cortex, occipital lobe, and corpus callosum. The components were negatively correlated with delay discounting, such that weaker loadings were associated with higher discounting. The component loadings were lower in persons with CUD, meaning the component was expressed less strongly. Our findings reveal structural and functional co-alterations linked to delay discounting, particularly in brain regions involved in reward salience, executive control, and visual attention and connecting white matter tracts. Importantly, these multimodal networks were weaker in persons with CUD, indicating less cognitive control that may contribute to impulsive behaviors.
机译:延迟折扣已提出作为物质使用障碍的行为标记。创新的分析方法,将来自多个神经影像模型的信息集成在一起可以为药物使用对大脑的复杂效果提供新的见解。本研究实施了监督的多模式融合方法,以揭示与延迟折扣相关的神经网络,使人们与可卡因使用障碍(CUD)分区。具有(n?=α35)的成年人(n?=Δ37)CUD完成了磁共振成像(MRI)扫描以获取高分辨率解剖,休息状态功能和扩散加权图像。每个数据模型的预计算机特征包括分别用于灰质体积,分数各向异性和区域均匀性的全脑体素 - 方面图。随着延迟折扣作为参考,多峰典型分量分析加联合独立分量分析来识别脑结构和功能的共同改变。该样本为58%男性和78%的非洲裔美国人。正如预期的那样,与没有CUD的人相比,CUD的参与者具有更高的延迟折扣。鉴定了一个联合组分,与所有方式的延迟折扣相关,涉及丘脑中的地区,背体纹状体,突然高压面皮,枕骨叶和胼callosum。组件与延迟折扣负相关,使得较弱的负荷与更高的折扣相​​关。用CUD的人的组分载荷较低,这意味着组分的表达不太强烈。我们的研究结果揭示了与延迟折扣相关的结构和功能的共同改变,特别是在奖励显着,执行控制和视觉关注和连接白质子的脑区。重要的是,这些多模态网络与CUD的人员较弱,表明可能导致冲动行为的认知控制较少。

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