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Exploring the long-term impact of early life adversity on the (anti-)social brain

Subject Area Clinical Psychiatry, Psychotherapy, Child and Adolescent Psychiatry
Term from 2017 to 2022
Project identifier Deutsche Forschungsgemeinschaft (DFG) - Project number 378004674
 
Final Report Year 2023

Final Report Abstract

The aim of the project was to elucidate the neural and behavioral correlates of environmental risk and protective factors. To this aim, we assessed multimodal data including neuroimaging, e-diaries, clinical interviews and questionnaires in a longitudinal study following adult participants at risk since birth (“Mannheim Study of Children at Risk (MARS)”; n=256). In addition, we used existing data from clinical and population-based cohorts and performed metaanalyses. From a risk side, we thereby provided meta-analytic evidence for early (social) adversity-related functional alterations in the superior frontal gyrus, the amygdala, the putamen and the precuneus and for decreased coupling of the amygdala with the anterior cingulate cortex (ACC) and the hippocampus. These findings were mirrored on a structural level confirming the susceptibility of the amygdala and the perigenual ACC volume to early social adversity. Capitalizing on the MARS data set, we provided evidence that early but not later life stress in infancy predicted prefrontal cortical thickness reductions and increased depressive symptoms. Further, we showed that whole-brain based structural alterations as a function of lifespan adversity are widespread and stable during adulthood as well as replicable in an independent cohort. At the individual level, deviations from this pattern were predictive of anxiety. Additional support for the clinical relevance of individual deviations from the normative neurodevelopment, specifically with respect to aggression, was provided in a sample of patients with disruptive behavior and healthy controls. Considering functional data, we showed that a (social) adversity background is related to dysfunctional cognitive and affective processing, reflected in a lower modulation of prefrontal and striatal brain activity by expected value and prediction error during reward-based decision making, increased ACC sensitivity during rejection, and lower regulatory prefrontal activity and whole-brain-based coupling during emotion regulation. With regard to resilience, we demonstrated a differential predictive value of affective and cognitive prefrontal control when confronted with immediate and sustained stress, respectively. Moreover, empathy –related activity in the precuneus and the temporoparietal junction predicted negative affect during the pandemic, particularly in participants with early psychosocial risks. Considering the social environment, we found evidence for momentary affective benefit after social interactions before and during the COVID-19 lockdown. This was shown in vivo (face-toface) only and not with respect to digital interactions and was moderated by the amygdala, genetic risk and personality. A long-term risk-counteracting effect of favorable early social interactions, in particular early maternal care, was further revealed regarding ADHD, reward and emotion processing. In sum, our results highlight the short- as well as long-term adverse and protective effects of the social environment on psychopathology and well-being in general. These effects extend to various brain structures, including the limbic and striatal system, as well as prefrontal regulatory instances. Further, the findings highlight that adversity-related structural alterations are widespread, are stable through adulthood, and replicable in an independent cohort. In terms of brain-behavior relationships, regulatory and emotive brain activity was predictive for well-being under stress and we show that individual deviations from normative models might be a promising future avenue to investigate brain-behavioral phenotype associations.

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