White matter abnormalities in depression: A categorical and phenotypic diffusion MRI study
White matter abnormalities in depression: A categorical and phenotypic diffusion MRI study
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DOI：
10.1016/j.nicl.2019.101710
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发表时间：
2019-01-01
影响因子：
4.2
通讯作者：
Drapier, Dominique
中科院分区：
文献类型：
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作者：
Coloigner, Julie;Batail, Jean-Marie;Drapier, Dominique
心境抑郁障碍是最致残的慢性疾病之一，其日常生活残疾率很高，影响全球3.5亿人。神经影像学的最新进展已经报道了广泛的结构异常，提示功能障碍的额叶-边缘系统回路参与了抑郁症的病理生理机制。然而，各种不同的白色物质区域已经被牵涉，并且试图遭受缺乏这种基于分类的生物标志物的再现性。这些不一致的结果可能归因于多种因素：抑郁症的实际分类定义以及临床表型的变异性。在这项研究中，我们1/检查了一个大型队列（114例患者）与健康对照组相比的WM变化，2/试图确定与特定抑郁表型相关的特定WM改变，如快感缺乏（即缺乏快乐），焦虑和精神发育迟滞-抑郁症的三个核心症状。与先前的研究一致，在胼胝体延伸至下束和后丘脑辐射的胼胝体内观察到减少的白色物质，证实了额叶-边缘回路异常。我们的分析还报告了其他模式的各向异性分数和轴向扩散率增加，以及减少的表观扩散系数和径向扩散率在压部的胼胝体和后肢的内囊。此外，FA与快感缺乏在上级纵束呈正相关，在扣带呈负相关。然后，焦虑和扩散度量的分析显示，焦虑增加与更大的FA值在胼胝体，前放射冠和后丘脑放射的背侧和压部。最后，运动发育迟缓分析显示Widlocher抑郁发育迟缓量表评分增加与身体FA减少以及胼胝体、穹窿和上级纹状体减少相关。通过这种双重方法（分类和表型），这项研究强调了向基于生物标志物的生物标志物研究领域迈进的必要性，这有助于了解心境抑郁障碍的病理生理学，并通过有针对性的治疗策略对抑郁症的精确表型进行分层。
Mood depressive disorder is one of the most disabling chronic diseases with a high rate of everyday life disability that affects 350 million people around the world. Recent advances in neuroimaging have reported widespread structural abnormalities, suggesting a dysfunctional frontal-limbic circuit involved in the pathophysiological mechanisms of depression. However, a variety of different white matter regions has been implicated and is sought to suffer from lack of reproducibility of such categorical-based biomarkers. These inconsistent results might be attributed to various factors: actual categorical definition of depression as well as clinical phenotype variability. In this study, we 1/ examined WM changes in a large cohort (114 patients) compared to a healthy control group and 2/ sought to identify specific WM alterations in relation to specific depressive phenotypes such as anhedonia (i.e. lack of pleasure), anxiety and psychomotor retardation -three core symptoms involved in depression. Consistent with previous studies, reduced white matter was observed in the genu of the corpus callosum extending to the inferior fasciculus and posterior thalamic radiation, confirming a frontal-limbic circuit abnormality. Our analysis also reported other patterns of increased fractional anisotropy and axial diffusivity as well as decreased apparent diffusion coefficient and radial diffusivity in the splenium of the corpus callosum and posterior limb of the internal capsule. Moreover, a positive correlation between FA and anhedonia was found in the superior longitudinal fasciculus as well as a negative correlation in the cingulum. Then, the analysis of the anxiety and diffusion metric revealed that increased anxiety was associated with greater FA values in genu and splenium of corpus callosum, anterior corona radiata and posterior thalamic radiation. Finally, the motor retardation analysis showed a correlation between increased Widlocher depressive retardation scale scores and reduced FA in the body and genu of the corpus callosum, fornix, and superior striatum. Through this twofold approach (categorical and phenotypic), this study has underlined the need to move forward to a symptom-based research area of biomarkers, which help to understand the pathophysiology of mood depressive disorders and to stratify precise phenotypes of depression with targeted therapeutic strategies.