# Associations Among Cyberbullying Victimization, Inhibitory Control, Neural Activation of Error Processing, and Mental Health Problems in Adolescents: Neuroimaging, Retrospective Longitudinal Cohort Study Using the Adolescent Brain Cognitive Development Data

**Authors:** Xuanyu Zhang, Chengyan Xie, Yu Chen, Boyu Qiu

PMC · DOI: 10.2196/75126 · 2026-02-18

## TL;DR

This study finds that cyberbullying in early adolescence is linked to increased externalizing problems and changes in brain activity related to error processing in later years.

## Contribution

The study provides longitudinal neuroimaging evidence of altered brain activation in cyberbullying victims during error processing.

## Key findings

- Cyberbullying at age 9-10 is associated with greater externalizing problems two years later.
- Cyberbullying is linked to increased neural activation in brain regions during error processing four years later.
- Neural changes do not directly mediate the link between cyberbullying and externalizing problems.

## Abstract

Cyberbullying victimization is prevalent and closely linked to mental health problems. However, existing research, often limited by cross-sectional designs and a focus on direct relationships, has yielded inconsistent results. Furthermore, the biological mechanisms underlying the relationship between cyberbullying victimization and psychopathological outcomes remain largely unclear at present.

This retrospective cohort study aimed to explore the longitudinal associations among cyberbullying victimization, inhibitory control, brain activation during error processing, and mental health problems among adolescents.

We curated the clinical, behavioral, and neuroimaging data (551/1186, 46.5% girls; 9-10 years at baseline) from the Adolescent Brain Cognitive Development study, a nationally representative cohort established through school-based probability sampling (selected factors included gender, race/ethnicity, socioeconomic status, and urbanicity). Participants were assessed by the cyberbullying question, the functional magnetic resonance imaging stop signal task for inhibitory control and error processing, and the Child Behavioral Checklist for externalizing and internalizing problems at 2-year (T1) and 4-year follow-up (T2). Linear mixed models were used to examine the retrospective longitudinal associations between these clinical, behavioral, and neuroimaging factors.

Linear mixed models showed that victims of cyberbullying at T1 exhibited significantly greater externalizing problems at T2 (β=0.25, 95% CI 0.06-0.45, PFDR=.02), but not for internalizing problems (β=–0.01, 95% CI –0.20 to 0.19, PFDR=.99) or deficits in inhibitory control (Correct Stop Rate: β=–0.02, 95% CI –0.26 to 0.21, PFDR=.85; Stop Signal Reaction Time: β=–0.07, 95% CI –0.27 to 0.13, PFDR=.85). Furthermore, cyberbullying victimization at T1 contributed to higher activation in the bilateral superior parietal gyri (left: β=0.36, 95% CI 0.10-0.61, PFDR=.04; right: β=0.34, 95% CI 0.08-0.59, PFDR=.04), right inferior parietal gyrus (β=0.32, 95% CI 0.07-0.57, PFDR=.04), and right posterior cingulate cortex (β=0.34, 95% CI 0.09-0.60, PFDR=.04) during error processing at T2. However, these neural alterations did not significantly mediate between cyberbullying victimization at T1 and externalizing problems at T2.

This longitudinal functional magnetic resonance imaging study investigates neural correlates of cyberbullying victimization in adolescents. By extending prior research that has relied primarily on cross-sectional or behavioral data, this research demonstrates that this form of victimization is associated with altered neural activation during error processing in later development. The pattern of nonsignificant impairment in inhibitory control and mediation to externalizing problems suggests that these neural impacts may be better characterized by a state of heightened sensitivity and compensatory engagement than by direct damage. Overall, this study points to the error-processing network as a potential target for cognitive interventions and establishes a foundation for further exploration of other neural mechanisms between cyberbullying victimization and mental health outcomes.

## Full-text entities

- **Genes:** AP2B1 (adaptor related protein complex 2 subunit beta 1) [NCBI Gene 163] {aka ADTB2, AP105B, AP2-BETA, CLAPB1}, APP (amyloid beta precursor protein) [NCBI Gene 351] {aka AAA, ABETA, ABPP, AD1, APPI, CTFgamma}, SST (somatostatin) [NCBI Gene 6750] {aka SMST, SST1}
- **Diseases:** Mental Health Problems (MESH:D000076082), Inhibitory control deficits (MESH:D007174), anxious depressive symptoms (MESH:D003866), aggressive tendencies (MESH:C536965), aggression (MESH:D010554), eating disorder (MESH:D001068), ABCD (MESH:D002658), Cognitive Development (MESH:D003072), externalizing and internalizing problems (MESH:D000082122), trauma (MESH:D014947), externalizing behaviors (MESH:D017577), sleep disturbance (MESH:D012893), mental (MESH:D008607), ACEs (MESH:D003643), neural damage (MESH:D015441), bullying (MESH:D000073397), anxiety (MESH:D001007), mental health disorders (OMIM:603663)
- **Chemicals:** cortisol (MESH:D006854)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Figures

2 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12961395/full.md

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Source: https://tomesphere.com/paper/PMC12961395