Life Sciences

Trajectories of cortical structures associated with stress across adolescence: a bivariate latent change score approach

Publié le - Journal of Child Psychology and Psychiatry

Auteurs : Tochukwu Nweze, Tobias Banaschewski, Cyracius Ajaelu, Chukwuemeka Okoye, Michael Ezenwa, Robert Whelan, Dimitri Papadopoulos Orfanos, Arun Bokde, Sylvane Desrivières, Antoine Grigis, Hugh Garavan, Penny Gowland, Andreas Heinz, Rüdiger Brühl, Jean-Luc Martinot, Marie-Laure Paillère Martinot, Eric Artiges, Frauke Nees, Tomáš Paus, Luise Poustka, Sarah Hohmann, Sabina Millenet, Juliane Fröhner, Michael Smolka, Henrik Walter, Gunter Schumann, Jamie Hanson, Arun L.W. Bokde

Background Stress exposure in childhood and adolescence has been linked to reductions in cortical structures and cognitive functioning. However, to date, most of these studies have been cross‐sectional, limiting the ability to make long‐term inferences, given that most cortical structures continue to develop through adolescence. Methods Here, we used a subset of the IMAGEN population cohort sample ( N = 502; assessment ages: 14, 19, and 22 years; mean age: 21.945 years; SD = 0.610) to understand longitudinally the long‐term interrelations between stress, cortical development, and cognitive functioning. To these ends, we first used a latent change score model to examine four bivariate relations – assessing individual differences in change in the relations between adolescent stress exposure and volume, surface area, and cortical thickness of cortical structures, as well as cognitive outcomes. Second, we probed for indirect neurocognitive effects linking stress to cortical brain structures and cognitive functions using rich longitudinal mediation modeling. Results Latent change score modeling showed that greater baseline adolescence stress at age 14 predicted a small reduction in the right anterior cingulate volume (Std. β = −.327, p = .042, 95% CI [−0.643, −0.012]) and right anterior cingulate surface area (Std. β = −.274, p = .038, 95% CI [−0.533, −0.015]) across ages 14–22. These effects were very modest in nature and became nonsignificant after correcting for multiple comparisons. Our longitudinal analyses found no evidence of indirect effects in the two neurocognitive pathways linking adolescent stress to brain and cognitive outcomes. Conclusion Findings shed light on the impact of stress on brain reductions, particularly in the prefrontal cortex that have consistently been implicated in the previous cross‐sectional studies. However, the magnitude of effects observed in our study is smaller than that has been reported in past cross‐sectional work. This suggests that the potential impact of stress during adolescence on brain structures may likely be more modest than previously noted.