ArticleScientific reports2025
Neuroticism modulates functional connectivity of the midcingulate cortex during emotional conflict.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- The mediating effect of neuroticism on the association between brain signal variability in the prefrontal cortex and depression among healthy individuals.Brain imaging and behavior · 2026Article
- Neural Mechanisms of Neuroticism: Large-Scale Brain Networks, Developmental Trajectories, and Translational Implications.Brain sciences · 2026Review
- The Big Five Personality Traits and Self-Management in Chronic Disease: A Scoping Review of Mediating Pathways.Psychology research and behavior management · 2026Review
- Abnormal Resting-State Functional Connectivity Between the Dorsal Anterior Cingulate Cortex and the Limbic System Contributes to Pain and Emotion Regulation Impairment in Fibromyalgia Patients.International journal of rheumatic diseases · 2026Article
- The role of amygdala reactivity in affective fluctuations across social contexts.Scientific reports · 2025Article
- Frontocortical activity and emotional experience in the context of daily life events.Social cognitive and affective neuroscience · 2025Article
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Authors and funding
5 authors.
Funding
Abstract
Neuroticism (NT) is a fundamental personality trait and a major risk factor for both the onset and persistence of depression and anxiety disorders. Although NT involves alterations in emotion-cognition interaction, its precise neural mechanism remains insufficiently understood. Leveraging the word-face Stroop task, we examined neural circuits engaged during emotional conflict using a relatively large sample that exhibited a wide range of NT levels. Generalized psychophysiological interaction (gPPI) analyses revealed that individuals with high NT were characterized by decreased functional connectivity between the anterior midcingulate cortex (aMCC) and both the left dorsolateral prefrontal cortex (dlPFC) and the left amygdala. None of these regions showed modulated brain activation by NT. Our findings suggest that the neural substrates of NT can be better characterized by reduced top-down aMCC-amygdala regulation as well as inefficient communication within the dorsal cognitive system (aMCC-dlPFC), rather than changes in brain activation in isolated regions. These observations offer valuable insights into the neural markers of vulnerability to mood and anxiety disorders.
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