The aberrant salience hypothesis proposes that striatal dopamine dysregulation causes misattribution of salience to irrelevant stimuli leading to psychosis. Recently, new lines of preclinical evidence on information coding by subcortical dopamine coupled with computational models of the brain's ability to predict and make inferences about the world (predictive processing) provide a new perspective on this hypothesis. We review these and summarize the evidence for dopamine dysfunction, reward processing, and salience abnormalities in people at clinical high risk of psychosis (CHR) relative to findings in patients with psychosis. This review identifies consistent evidence for dysregulated subcortical dopamine function in people at CHR, but also indicates a number of areas where neurobiological processes are different in CHR subjects relative to patients with psychosis, particularly in reward processing. We then consider how predictive processing models may explain psychotic symptoms in terms of alterations in prediction error and precision signaling using Bayesian approaches. We also review the potential role of environmental risk factors, particularly early adverse life experiences, in influencing the prior expectations that individuals have about their world in terms of computational models of the progression from being at CHR to frank psychosis. We identify a number of key outstanding questions, including the relative roles of prediction error or precision signaling in the development of symptoms and the mechanism underlying dopamine dysfunction. Finally, we discuss how the integration of computational psychiatry with biological investigation may inform the treatment for people at CHR of psychosis.

中文翻译：

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临床精神病高危人群的异常显着性、信息处理和多巴胺能信号传导

异常显着性假说提出，纹状体多巴胺失调会导致显着性错误归因于不相关的刺激，从而导致精神病。最近，关于皮层下多巴胺信息编码的新临床前证据，加上大脑预测和推断世界的能力（预测处理）的计算模型，为这一假设提供了新的视角。我们回顾了这些并总结了临床高危精神病（CHR）人群中多巴胺功能障碍、奖励处理和显着性异常的证据，与精神病患者的研究结果相关。本综述确定了 CHR 患者皮层下多巴胺功能失调的一致证据，但也指出了 CHR 受试者与精神病患者的神经生物学过程在许多方面存在差异，特别是在奖励处理方面。然后，我们考虑预测处理模型如何使用贝叶斯方法根据预测误差和精确信号的变化来解释精神病症状。我们还回顾了环境风险因素的潜在作用，特别是早期不良生活经历，在影响个人对他们的世界的先前期望方面的潜在作用，从 CHR 到坦率精神病的进展的计算模型。我们确定了许多关键的悬而未决的问题，包括预测误差或精确信号在症状发展中的相对作用以及多巴胺功能障碍的机制。最后，我们讨论了计算精神病学与生物学研究的整合如何为 CHR 精神病患者的治疗提供信息。