Department of Psychiatry, Johns Hopkins University School of Medicine, 600 N. Wolfe Street, Baltimore, MD 21287, USA.
Russell H Morgan Department of Radiology and Radiological Sciences, Johns Hopkins University School of Medicine, 1550 Orleans Street, Baltimore, MD 21231, USA.
Schizophr Res. 2018 Jul;197:492-497. doi: 10.1016/j.schres.2018.01.015. Epub 2018 Feb 3.
Changes in inflammatory cascades have been implicated in the underlying pathophysiology of psychosis. Translocator protein 18 kDa (TSPO) has been used to assess neuroinflammatory processes in psychotic disorders. Nonetheless, it is unclear whether TSPO, a mitochondrial protein, can be interpreted as a general marker for inflammation in diseases involving psychosis. To address this question, we investigated TSPO signaling in representative mouse models for psychosis with inflammatory disturbances. The maternal immune activation and cuprizone short-term exposure models show different TSPO signaling. Furthermore, we observed similarities and differences in their respective stress pathways including stress hormone signaling and oxidative stress that are functionally interconnected with the inflammatory responses. We propose that more careful studies of TSPO distribution in neuroinflammation and other stress cascades associated with psychotic symptoms will allow us to understand the biological mechanisms underlying psychosis-related behaviors.
炎症级联反应的变化与精神病学的潜在病理生理学有关。转位蛋白 18kDa（TSPO）已被用于评估精神疾病的神经炎症过程。然而，TSPO 作为一种线粒体蛋白，是否可以被解释为涉及精神病的炎症的一般标志物，目前尚不清楚。为了解决这个问题，我们研究了具有炎症障碍的代表性精神病学小鼠模型中的 TSPO 信号。母体免疫激活和铜缺乏短期暴露模型显示出不同的 TSPO 信号。此外，我们观察到它们各自的应激途径中的相似性和差异性，包括应激激素信号和与炎症反应功能相关的氧化应激。我们提出，更仔细地研究 TSPO 在神经炎症中的分布以及与精神病症状相关的其他应激级联反应，将使我们能够理解精神病相关行为的生物学机制。
