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Increased Default Mode Network Connectivity and Temperament Predict Internalizing Symptoms in Early Childhood

Halle Miller, Johanna Chajes, Tobias Grossmann

preprint DOI: 10.21203/rs.3.rs-7528043/v1 (opens in new tab)

Study at a glance

AI-extracted from the abstract
Characteristics Observational cohort
Population Typically developing children aged 4 to 6 years from a community sample
Topics Default mode network
Key findings Greater default mode network connectivity, higher negative affect, and lower surgency were significant independent predictors of internalizing symptoms in early childhood.

Abstract

Abstract This study investigates the early neural and temperament precursors to internalizing psychopathology. Increased default mode network (DMN) functional connectivity and decreased frontoparietal network (FPN) connectivity are established neural signatures of internalizing disorders in adults, but it is unknown if these patterns represent early-emerging vulnerability. In a community sample of typically developing children aged 4 to 6 years, we examined the concurrent predictive power of resting-state functional connectivity and temperament for internalizing symptoms. We hypothesized that increased DMN connectivity, decreased FPN connectivity, and temperament traits of high negative affect and low surgency would predict higher internalizing problems. Functional connectivity was measured using functional near-infrared spectroscopy (fNIRS), a child-friendly neuroimaging technique. Internalizing symptoms and temperament were assessed via parent report using the Child Behavior Checklist and Child Behavior Questionnaire, respectively. A multiple linear regression revealed that greater DMN connectivity, higher negative affect, and lower surgency were significant, independent predictors of internalizing symptoms. FPN connectivity was not a significant predictor. These findings suggest that a key neural signature of adult depression—DMN hyperconnectivity—is already associated with subclinical symptoms in early childhood, supporting its role as a primary vulnerability marker. The absence of an FPN association likely reflects the protracted maturation of this cognitive control network, pointing to a developmental lag in the emergence of distinct neural risk factors for internalizing disorders.