ArticleDevelopment and psychopathology2025
Leveraging bifactor modeling to test prospective direct and indirect effects of adolescent alcohol use and externalizing symptoms on the development of task-general executive functioning.
Article in Development and psychopathology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Childhood Material Hardship Linked to Adolescent Neurocognition: A Computational Modeling Approach.Developmental science · 2026Article
- Behavioral Disinhibition Model of Addiction: A Review and New Findings from the Minnesota Twin Family Study.Behavior genetics · 2026Review
- Sex Differences in the Association Between Drinking Motives, Protective Behavioral Strategies, and Alcohol Outcomes in a Hazardous Drinking College Sample.Substance use & misuse · 2026Article
- Associations of Low-Level Prenatal Alcohol and Cannabis Exposure With Adolescent Cognitive Trajectories.Alcohol, clinical & experimental research · 2026Article
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Authors and funding
7 authors.
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Abstract
Adolescence is a period of substantial maturation in brain regions underlying Executive Functioning (EF). Adolescence is also associated with initiation and escalation of Alcohol Use (AU), and adolescent AU has been proposed to produce physiological and neurobiological events that derail healthy EF development. However, support has been mixed, which may be due to (1) failure to consider co-occurring externalizing symptoms (including other drug use) and poor social adaptation, and (2) heterogeneity and psychometric limitations in EF measures. We aimed to clarify the AU-EF association by: (1) distinguishing general externalizing symptoms from specific symptoms (AU, aggression, drug use) using bifactor modeling, (2) testing prospective associations between general externalizing symptoms and specific symptoms, and task-general EF, as indexed by a well-validated computational modeling framework (diffusion decision model), and (3) examining indirect pathways from externalizing symptoms to deficits in task-general EF through poor social adaptation. A high-risk longitudinal sample (
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