FKBP5 as a possible moderator of the psychosis-inducing effects of childhood trauma
FKBP5 as a possible moderator of the psychosis-inducing effects of childhood trauma
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DOI：
10.1192/bjp.bp.112.115972
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发表时间：
2013-04-01
影响因子：
10.5
通讯作者：
van Winkel, Ruud
中科院分区：
文献类型：
--
作者：
Collip, Dina;Myin-Germeys, Inez;van Winkel, Ruud
FK 506结合蛋白5（FKBP 5）是创伤后应激障碍（PTSD）和儿童期创伤后抑郁症的重要决定因素，目的研究FKBP 5创伤相互作用在部分应激相关精神病表型中的作用。并在不同家族倾向的三个样本中进行精神病模型随访（175个对照，200名未受影响的兄弟姐妹和195名精神病患者）。结果最一致的发现是在双胞胎样本中儿童创伤和rs 9296158/rs 4713916对精神病症状和皮质醇的相互作用，与兄弟姐妹（rs 4713916）和患者（rs 9296158），A-等位基因携带者在这两个多态性是最容易受到traumatic.ConclusionsTrauma可能会增加精神病的风险，通过持久的皮质醇反馈回路的变化，类似于创伤后应激障碍，提示精神病跨诊断界限可比的生物学机制。
BackgroundFK506 binding protein 5 (FKBP5) has repeatedly been shown to be a critical determinant of post-traumatic stress disorder (PTSD) and depression following childhood trauma.AimsTo examine the role of FKBP5 trauma interactions in the partly stress-related psychosis phenotype.MethodIn 401 general population twins, four functional polymorphisms were examined in models of psychosis and cortisol, and followed up in models of psychosis in three samples at different familial liability (175 controls, 200 unaffected siblings and 195 patients with a psychotic disorder).ResultsThe most consistent finding was an interaction between childhood trauma and rs9296158/rs4713916 on psychotic symptoms and cortisol in the twin sample, combined with a directionally similar interaction in siblings (rs4713916) and patients (rs9296158), A-allele carriers at both polymorphisms being most vulnerable to trauma.ConclusionsTrauma may increase the risk of psychosis through enduring changes in the cortisol feedback loop, similar to that for PTSD, suggesting comparable biological mechanisms for psychosis across diagnostic boundaries.