Department of Neuroimaging, Institute of Psychiatry, Psychology and Neuroscience, King's College London, United Kingdom.
Department of Neuroimaging, Institute of Psychiatry, Psychology and Neuroscience, King's College London, United Kingdom.
Biol Psychiatry Cogn Neurosci Neuroimaging. 2021 Jul;6(7):716-724. doi: 10.1016/j.bpsc.2020.12.017. Epub 2021 Jan 28.
Immune mechanisms have been implicated in the pathogenesis of depression. Translocator protein (TSPO)-targeted positron emission tomography (PET) has been used to assess neuroinflammation in major depressive disorder. We aimed to 1) test the hypothesis of significant case-control differences in TSPO binding in the anterior cingulate cortex, prefrontal cortex, and insula regions; and 2) explore the relationship between cerebral TSPO binding and peripheral blood C-reactive protein (CRP) concentration.
A total of 51 depressed subjects with Hamilton Depression Rating Scale score >13 (median 17; interquartile range, 16-22) and 25 healthy control subjects underwent dynamic brain C-PK11195 PET and peripheral blood immune marker characterization. Depressed subjects were divided into high CRP (>3 mg/L; n = 20) and low CRP (<3 mg/L; n = 31).
Across the three regions, TSPO binding was significantly increased in depressed versus control subjects (η = .09; F = 6.97, p = .01), which was not influenced by body mass index. The case-control difference was greatest in the anterior cingulate cortex (d = 0.49; t = 2.00, p = .03) and not significant in the prefrontal cortex or insula (d = 0.27 and d = 0.36, respectively). Following CRP stratification, significantly higher TSPO binding was observed in low-CRP depression compared with controls (d = 0.53; t = 1.96, p = .03). These effect sizes are comparable to prior major depressive disorder case-control TSPO PET data. No significant correlations were observed between TSPO and CRP measures.
Consistent with previous findings, there is a modest increase in TSPO binding in depressed patients compared with healthy control subjects. The lack of a significant correlation between brain TSPO binding and blood CRP concentration or body mass index poses questions about the interactions between central and peripheral immune responses in the pathogenesis of depression.
免疫机制与抑郁症的发病机制有关。 用于评估重度抑郁症神经炎症的 translocator 蛋白 (TSPO) 靶向正电子发射断层扫描 (PET) 已被用于评估重度抑郁症的神经炎症。 我们的目的是：1）检验在前扣带回皮质、前额叶皮质和脑岛区域 TSPO 结合存在显著病例对照差异的假设；2）探索大脑 TSPO 结合与外周血 C 反应蛋白 (CRP) 浓度之间的关系。
共有 51 名汉密尔顿抑郁评定量表评分>13 分（中位数 17；四分位间距 16-22）的抑郁患者和 25 名健康对照者接受了动态脑 C-PK11195 PET 和外周血免疫标志物特征分析。 将抑郁患者分为高 CRP (>3mg/L；n=20) 和低 CRP (<3mg/L；n=31)。
在三个区域，与对照组相比，抑郁患者的 TSPO 结合显著增加（η=0.09；F=6.97，p=0.01），而这不受体重指数的影响。 在前扣带回皮质（d=0.49；t=2.00，p=0.03）的病例对照差异最大，在前额叶皮质或脑岛差异不显著（d=0.27 和 d=0.36）。 在 CRP 分层后，与对照组相比，低 CRP 抑郁症患者的 TSPO 结合显著增加（d=0.53；t=1.96，p=0.03）。 这些效应大小与先前的重度抑郁症病例对照 TSPO PET 数据相当。 未观察到 TSPO 与 CRP 测量之间存在显著相关性。
与先前的发现一致，与健康对照组相比，抑郁患者的 TSPO 结合略有增加。 大脑 TSPO 结合与血液 CRP 浓度或体重指数之间没有显著相关性，这对抑郁症发病机制中中枢和外周免疫反应之间的相互作用提出了质疑。
