Reduced fractional anisotropy in patients with major depressive disorder and associations with vascular stiffness.

Reduced fractional anisotropy in patients with major depressive disorder and associations with vascular stiffness.
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严重抑郁症患者的分数各向异性降低,并与血管僵硬相关。

DOI:
10.1016/j.nicl.2017.01.013
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发表时间:
2017
期刊:
NeuroImage. Clinical
影响因子:
--
通讯作者:
Wersching H
Wersching H
中科院分区:
其他
文献类型:
--
作者:
Hermesdorf M;Berger K;Szentkirályi A;Schwindt W;Dannlowski U;Wersching H

文献摘要

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先前的研究揭示了重度抑郁症患者大脑白质的一些变化。然而,尚不清楚这些变化是否与大脑和其他身体部位的血管变化有关。我们通过基于束的空间统计方法,比较了具有明确特征的中年重度抑郁症患者 (n = 290) 和非抑郁对照 (n = 346) 样本中的扩散张量成像衍生的分数各向异性。随后,在提取的分数各向异性估计值中,分析了脉搏波速度作为抑郁症和年龄相关变化的中介的潜在作用。基于束的分析结果显示,与抑郁症相关的左后丘脑辐射各向异性分数显着降低。对提取数据的分析表明,后丘脑辐射和左侧矢状层的双边各向异性分数进一步减少。间接影响的分析没有显示抑郁相关影响通过脉搏波速度对分数各向异性的任何显着调节。然而,与年龄相关的各向异性分数的影响部分是由脉搏波速度介导的。总之,重度抑郁症与对脑白质微结构特性的有害影响有关,这些影响与通过脉搏波速度测量的血管变化无关。然而,与年龄相关的对白质的部分有害影响可以用血管变化来解释。需要进行纵向研究来调查白质和血管参数随时间的变化及其与抑郁症的关联。抑郁症与丘脑后辐射和矢状层的分数各向异性减少有关。脉搏波速度与大脑白质各向异性分数的降低有关。脉搏波速度不会介导抑郁相关的白质微结构影响。脉搏波速度介导了与年龄相关的对白质微观结构的部分有害影响。
Previous studies revealed several alterations of the cerebral white matter in patients with major depressive disorder. However, it is unknown if these alterations are associated with vascular changes in the brain and other body parts. We compared diffusion tensor imaging derived fractional anisotropy in a well characterized sample of middle-aged patients with major depressive disorder (n = 290) and never-depressed controls (n = 346) by the method of tract-based spatial statistics. Subsequently, the potential role of pulse wave velocity as a mediator of depression- and age-related changes in extracted estimates of fractional anisotropy were analyzed. The results of the tract-based analysis revealed significantly reduced fractional anisotropy in the left posterior thalamic radiation associated with depression. Analyses of extracted data indicated additional reductions of fractional anisotropy bilaterally in the posterior thalamic radiation and in the left sagittal stratum. The analyses of indirect effects did not show any significant mediation of depression-related effects on fractional anisotropy via pulse wave velocity. However, age-related effects on fractional anisotropy were partially mediated by pulse wave velocity. In conclusion, major depressive disorder is associated with detrimental effects on cerebral white matter microstructure properties which are independent of vascular changes, as measured by pulse wave velocity. However, a portion of age-related detrimental effects on white matter is explained by vascular changes. Longitudinal studies are required for investigating changes in white matter and vascular parameters over time and their association with incident depression. Depression is associated with reduced fractional anisotropy in the posterior thalamic radiation and in the sagittal stratum. Pulse wave velocity is associated with reduced fractional anisotropy across the cerebral white matter. Pulse wave velocity does not mediate depression-related effects on white matter microstructure. Pulse wave velocity mediates a part of age-related detrimental effects on white matter microstructure.