<p>Adolescence is a period of rapid neurobiological and behavioural change, yet how brain maturation deviations relate to psychopathology remains unclear. Here, we show, using data from the Adolescent Brain Cognitive Development Study, that deviations in brain age are coupled with internalising and externalising symptom development across adolescence. Combining multimodal brain age prediction across four waves (ages ~8.3–17.5) with bivariate latent growth curve models of ten symptom waves, we found coordinated nonlinear development between brain maturation and symptoms: adolescents whose brains increasingly diverged from age-expected maturation showed increasing symptoms. Effects were most consistent for internalising symptoms in females (<i>r</i> = 0.15–0.23) and broader for externalising symptoms in both sexes (<i>r</i> = 0.15–0.32); intercept-level associations were weaker (<i>r</i> = 0.08–0.09). Sex differences were not robust after correction. Vulnerability to adolescent psychopathology appears more closely linked to changes in brain maturational tempo than to fixed differences in brain age.</p>

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Synchrony between brain age and internalising and externalising symptoms across adolescence

  • Dani Beck,
  • Chloe Carrick,
  • Eira R. Aksnes,
  • Niamh MacSweeney,
  • Lars T. Westlye,
  • Delia Fuhrmann,
  • Christian K. Tamnes

摘要

Adolescence is a period of rapid neurobiological and behavioural change, yet how brain maturation deviations relate to psychopathology remains unclear. Here, we show, using data from the Adolescent Brain Cognitive Development Study, that deviations in brain age are coupled with internalising and externalising symptom development across adolescence. Combining multimodal brain age prediction across four waves (ages ~8.3–17.5) with bivariate latent growth curve models of ten symptom waves, we found coordinated nonlinear development between brain maturation and symptoms: adolescents whose brains increasingly diverged from age-expected maturation showed increasing symptoms. Effects were most consistent for internalising symptoms in females (r = 0.15–0.23) and broader for externalising symptoms in both sexes (r = 0.15–0.32); intercept-level associations were weaker (r = 0.08–0.09). Sex differences were not robust after correction. Vulnerability to adolescent psychopathology appears more closely linked to changes in brain maturational tempo than to fixed differences in brain age.