Neuroticism modulates functional connectivity of the midcingulate cortex during emotional conflict

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.

Authors

Institutions

Publication Details

Journal
Scientific Reports
Published
2025-04-16
DOI
https://doi.org/10.1038/s41598-025-97529-8
Citations
3
Primary Topic
Functional Brain Connectivity Studies
Type
article
Field-Weighted Citation Impact
4.29
Controls
|||
ALL TIME
JAN
FEB
MAR
APR
MAY
JUN
JUL
AUG
SEP
OCT
article

Neuroticism modulates functional connectivity of the midcingulate cortex during emotional conflict

Juyoen Hur, Hakin Kim, Manuel Kuhn, M. Justin Kim et al.
3 citations
Scientific Reports
Functional Brain Connectivity Studies
4.29
article

Neuroticism modulates functional connectivity of the midcingulate cortex during emotional conflict

Juyoen Hur, Hakin Kim, Manuel Kuhn, M. Justin Kim, Junhyun Park
article en
3 citations

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.

Scientific ReportsVol. 15(1)
Harvard University (US), Yonsei University (KR), Institute for Basic Science (KR), Sungkyunkwan University (KR)
Reduced inequalities
Openalex Percentile: Top 7%
Functional Brain Connectivity Studies
4.29
AI Navigator

Ask Laika to Summarize, Analyze, and Connect papers live on the map.

Summarize Papers & Methodologies

Extract key findings, datasets, and comparative methods across publications.

Benchmark Rankings & Visual Analytics

Rank top research institutions, authors, funders, topics, and journals by Field-Weighted Citation Impact (FWCI) and paper volume with instant charts.

Connect Distant Disciplines

Bridge topological clusters on the map to find hidden collaborative intersections.

Neuroticism modulates functional connectivity of the midcingulate cortex during emotional conflict — Juyoen Hur, Hakin Kim, et al. · Scientific Reports (2025) | TGRS Research Map | TGRS