D V Atanassova, J M Oosterman, A O Diaconescu, C Mathys, V I Madariaga, I A Brazil
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引用次数: 0
Abstract
Impairments in reinforcement learning (RL) might underlie the tendency of individuals with elevated psychopathic traits to behave exploitatively, as they fail to learn from their mistakes. Most studies on the topic have focused on binary choices, while everyday functioning requires us to learn the value of multiple options. In this study, we evaluated the cognitive correlates of naturalistic foraging-type decision-making and their electrophysiological signatures in a community sample (n = 108) with varying degrees of psychopathic traits. Reinforcers with different salience were included in a foraging-type decision-making task. Recruitment of various cognitive processes was estimated with a computational model and electrophysiology, and the relationships to psychopathic traits were assessed. Higher Antisocial traits were associated with a bias towards expecting more volatility in the environment when high-salience reinforcers were used. Additionally, higher levels of Interpersonal traits were associated with reduced learning from personalized rewards, as evidenced by reductions in the prediction errors (PEs) about rate of change. Higher Affective traits were associated with lower PEs and aberrant learning from painful punishments. Lastly, the PEs about rate of change were reflected in the trial-wise trajectories of Feedback-Related Negativity event-related potentials. Together, our results point to the importance of volatility processing in understanding aberrant decision-making in relation to psychopathy, demonstrate the relationships between psychopathic traits and learning through reward and punishment, and emphasise the potentially more beneficial effect of personalized rewards and punishment for improving reinforcement-based decision-making in individuals with elevated psychopathic traits.
期刊介绍:
Psychiatry has suffered tremendously by the limited translational pipeline. Nobel laureate Julius Axelrod''s discovery in 1961 of monoamine reuptake by pre-synaptic neurons still forms the basis of contemporary antidepressant treatment. There is a grievous gap between the explosion of knowledge in neuroscience and conceptually novel treatments for our patients. Translational Psychiatry bridges this gap by fostering and highlighting the pathway from discovery to clinical applications, healthcare and global health. We view translation broadly as the full spectrum of work that marks the pathway from discovery to global health, inclusive. The steps of translation that are within the scope of Translational Psychiatry include (i) fundamental discovery, (ii) bench to bedside, (iii) bedside to clinical applications (clinical trials), (iv) translation to policy and health care guidelines, (v) assessment of health policy and usage, and (vi) global health. All areas of medical research, including — but not restricted to — molecular biology, genetics, pharmacology, imaging and epidemiology are welcome as they contribute to enhance the field of translational psychiatry.