Choroid plexus enlargement is associated with neuroinflammation and reduction of blood brain barrier permeability in depression.

Choroid plexus enlargement is associated with neuroinflammation and reduction of blood brain barrier permeability in depression.
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DOI:
10.1016/j.nicl.2021.102926
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发表时间:
2022
期刊:
NeuroImage. Clinical
影响因子:
--
通讯作者:
Veronese M
Veronese M
中科院分区:
其他
文献类型:
--
作者:
Althubaity N;Schubert J;Martins D;Yousaf T;Nettis MA;Mondelli V;Pariante C;Harrison NA;Bullmore ET;Dima D;Turkheimer FE;Veronese M

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与对照组相比,抑郁症患者的MRI衍生脉络丛体积增加。抑郁症患者脉络丛扩大与神经炎症和血脑屏障通透性降低有关。成像转录组CP体积和TSPO PET成像证实了参与神经炎症反应的几种途径的基因富集。脉络丛体积增加的机制尚不清楚,可能不是抑郁症特有的。近年来的研究表明,脉络丛(choroid plexus,CP)可能参与神经免疫轴,在中枢和外周炎症的相互作用中发挥作用。在这里,我们的目的是调查抑郁症的CP体积变化及其与炎症的关系。研究人员对来自Wellcome Trust NIMA联盟的51名抑郁症参与者(HDRS评分> 13)和25名年龄和性别匹配的健康对照(HC)进行了重新分析。所有参与者均接受了完整的外周细胞因子分析和同步[11 C] PK 11195 PET/结构MRI成像,分别用于测量神经炎症和CP体积。我们发现抑郁症受试者的CP体积显着大于HC(t(76)= +2.17),这与前扣带回皮质中的[11 C] PK 11195 PET结合正相关(r = 0.28,p = 0.02),前额叶皮层(r = 0.24,p = 0.04),岛叶皮质(r = 0.24,p = 0.04),但不与外周炎症标志物:CRP水平(r = 0.07,p = 0.53)、IL-6(r =-0.08,p = 0.61)和TNF-α(r =-0.06,p = 0.70)。CP体积与CP中的[11 C] PK 11195 PET结合相关(r = 0.34,p = 0.005)。整合来自艾伦人脑图谱的转录组学数据与描绘CP体积和PET成像之间的相关性的脑图谱发现,参与神经炎症反应的几种途径的基因显著富集。这一结果支持了这样的假设,即脑屏障的变化可能导致血液和CSF之间的溶质交换减少,扰乱脑内稳态,并最终导致抑郁症的炎症。鉴于CP异常最近在其他脑部疾病中被检测到,这些结果可能不是抑郁症特有的,可能会扩展到其他具有外周炎症成分的疾病。
MRI-derived choroid plexus volume is increased in patients with depression as compared to match-controls. Choroid plexus enlargement is associated with neuroinflammation and reduction of blood–brain barriers permeability in depression. Imaging transcriptomic CP volume and TSPO PET imaging confirms gene enrichment for several pathways involved in neuroinflammatory response. Mechanisms choroid plexus volume increase remain unknow and might not be specific to depression. Recent studies have shown that choroid plexuses (CP) may be involved in the neuro-immune axes, playing a role in the interaction between the central and peripheral inflammation. Here we aimed to investigate CP volume alterations in depression and their associations with inflammation. 51 depressed participants (HDRS score > 13) and 25 age- and sex-matched healthy controls (HCs) from the Wellcome Trust NIMA consortium were re-analysed for the study. All the participants underwent full peripheral cytokine profiling and simultaneous [11C]PK11195 PET/structural MRI imaging for measuring neuroinflammation and CP volume respectively. We found a significantly greater CP volume in depressed subjects compared to HCs (t(76) = +2.17) that was positively correlated with [11C]PK11195 PET binding in the anterior cingulate cortex (r = 0.28, p = 0.02), prefrontal cortex (r = 0.24, p = 0.04), and insular cortex (r = 0.24, p = 0.04), but not with the peripheral inflammatory markers: CRP levels (r = 0.07, p = 0.53), IL-6 (r = -0.08, p = 0.61), and TNF-α (r = -0.06, p = 0.70). The CP volume correlated with the [11C]PK11195 PET binding in CP (r = 0.34, p = 0.005). Integration of transcriptomic data from the Allen Human Brain Atlas with the brain map depicting the correlations between CP volume and PET imaging found significant gene enrichment for several pathways involved in neuroinflammatory response. This result supports the hypothesis that changes in brain barriers may cause reduction in solute exchanges between blood and CSF, disturbing the brain homeostasis and ultimately contributing to inflammation in depression. Given that CP anomalies have been recently detected in other brain disorders, these results may not be specific to depression and might extend to other conditions with a peripheral inflammatory component.
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影响因子: 34.7
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