Publications by authors named "Paus T"

The evidence supporting the presence of individual brain structure correlates of the externalizing spectrum (EXT) is sparse and mixed. To date, large-sample studies of brain-EXT relations have mainly found null to very small effects by focusing exclusively on either EXT-related personality traits (e.g.

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Unhealthy eating, a risk factor for eating disorders (EDs) and obesity, often coexists with emotional and behavioral problems; however, the underlying neurobiological mechanisms are poorly understood. Analyzing data from the longitudinal IMAGEN adolescent cohort, we investigated associations between eating behaviors, genetic predispositions for high body mass index (BMI) using polygenic scores (PGSs), and trajectories (ages 14-23 years) of ED-related psychopathology and brain maturation. Clustering analyses at age 23 years ( = 996) identified 3 eating groups: restrictive, emotional/uncontrolled and healthy eaters.

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Background And Aim: Cannabis use disorder (CUD) is strongly influenced by genetic factors; however the mechanisms underpinning this association are not well understood. This study investigated whether a polygenic risk score (PRS) based on a genome-wide association study for CUD in adults predicts cannabis use in adolescents and whether the association can be explained by inter-individual variation in structural properties of brain white matter or risk-taking behaviors.

Design And Setting: Longitudinal and cross-sectional analyses using data from the IMAGEN cohort, a European longitudinal study integrating genetic, neuroimaging and behavioral measures.

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Copy-number variants (CNVs) that increase the risk for neurodevelopmental disorders also affect cognitive ability. However, such CNVs remain challenging to study due to their scarcity, limiting our understanding of gene-dosage-sensitive biological processes linked to cognitive ability. We performed a genome-wide association study (GWAS) in 258,292 individuals, which identified-for the first time-a duplication at 2q12.

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Introduction: A growing literature has shown that exposure to adverse life events during childhood or adolescence is associated with the presence of psychotic-like experiences (PLEs), which is in turn associated with the risk of psychotic outcomes. Ruminative thinking, i.e.

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  • - White matter hyperintensities indicate damage in the brain's white matter, which can lead to brain shrinkage and is linked to dementia; a study of over 51,000 people found that larger volumes of these hyperintensities correspond to thinner brain cortex.
  • - Researchers identified 20 significant genetic loci related to white matter hyperintensities that affect genes involved in brain cell types known to support vascular health and neuronal function; some of these genes play roles in processes like axonal structure and transport within the brain.
  • - The genetic traits tied to white matter issues were linked to cardiovascular health, neurodegeneration markers, and poorer cognitive performance, with a polygenic risk score effectively predicting dementia risk in a separate large
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  • Subcortical brain structures play a crucial role in various developmental and psychiatric disorders, and a study analyzed brain volumes in 74,898 individuals, identifying 254 genetic loci linked to these volumes, which accounted for up to 35% of variation.
  • The research included exploring gene expression in specific neural cell types, focusing on genes involved in intracellular signaling and processes related to brain aging.
  • The findings suggest that certain genetic variants not only influence brain volume but also have potential causal links to conditions like Parkinson’s disease and ADHD, highlighting the genetic basis for risks associated with neuropsychiatric disorders.
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  • Subcortical brain structures play a crucial role in various disorders, and a study analyzed the genetic basis of brain volumes in nearly 75,000 individuals of European ancestry, revealing 254 loci linked to these volumes.
  • The research identified significant gene expression in neural cells, relating to brain aging and signaling, and found that polygenic scores could predict brain volumes across different ancestries.
  • The study highlights genetic connections between brain volumes and conditions like Parkinson's disease and ADHD, suggesting specific gene expression patterns could be involved in neuropsychiatric disorders.
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  • - The study examined the impact of prenatal green space exposure on mental health in adolescents, using data from a Dutch cohort of 1,476 individuals and assessing outcomes like externalizing/internalizing problems, tobacco, and alcohol use.
  • - Results indicated that more prenatal green space was linked to higher externalizing problems; however, this association weakened when considering factors like urban living, and changes in green space during childhood showed a more positive impact on mental health.
  • - Overall, the findings suggest that prenatal green space exposure does not benefit adolescent mental health, but rather, increased green space during childhood may help reduce externalizing issues in early adolescence.
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Human brain morphology undergoes complex changes over the lifespan. Despite recent progress in tracking brain development via normative models, current knowledge of underlying biological mechanisms is highly limited. We demonstrate that human cortical thickness development and aging trajectories unfold along patterns of molecular and cellular brain organization, traceable from population-level to individual developmental trajectories.

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  • * It analyzed over 1000 participants from ages 14 to 23 to determine if issues with sustained attention predict future substance use rather than being just a side effect.
  • * The results showed that strong brain connections related to sustained attention at age 14 can predict an increase in cannabis and cigarette use later, highlighting sustained attention as a key indicator of vulnerability to substance use.
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During adolescence, cannabis experimentation is common, and its association with interindividual variations in brain maturation well studied. Cellular and molecular underpinnings of these system-level relationships are, however, unclear. We thus conducted a three-step study.

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Incomplete Hippocampal Inversion (IHI), sometimes called hippocampal malrotation, is an atypical anatomical pattern of the hippocampus found in about 20% of the general population. IHI can be visually assessed on coronal slices of T1 weighted MR images, using a composite score that combines four anatomical criteria. IHI has been associated with several brain disorders (epilepsy, schizophrenia).

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This chapter describes basic principles and key findings regarding the development and maturation of the human brain, the former referring to the pre-natal and early post-natal periods and the latter concerning childhood and adolescence. In both cases, we focus on brain structure as revealed in vivo with multi-modal magnetic resonance imaging (MRI). We begin with a few numbers about the human brain and its cellular composition and a brief overview of a number of MRI-based metrics used to characterize age-related variations in grey and white matter.

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Measures of physical growth, such as weight and height have long been the predominant outcomes for monitoring child health and evaluating interventional outcomes in public health studies, including those that may impact neurodevelopment. While physical growth generally reflects overall health and nutritional status, it lacks sensitivity and specificity to brain growth and developing cognitive skills and abilities. Psychometric tools, e.

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Adolescents exhibit remarkable heterogeneity in the structural architecture of brain development. However, due to limited large-scale longitudinal neuroimaging studies, existing research has largely focused on population averages, and the neurobiological basis underlying individual heterogeneity remains poorly understood. Here we identify, using the IMAGEN adolescent cohort followed up over 9 years (14-23 y), three groups of adolescents characterized by distinct developmental patterns of whole-brain gray matter volume (GMV).

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Perseverative negative thoughts, known as rumination, might arise from emotional challenges and preclude mental health when transitioning into adulthood. Due to its multifaceted nature, rumination can take several ruminative response styles, that diverge in manifestations, severity, and mental health outcomes. Still, prospective ruminative phenotypes remain elusive insofar.

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  • - The study investigates how the balance between excitation and inhibition in brain cortex microcircuits changes during adolescence, a critical period for brain maturation.
  • - Using advanced simulations and resting-state fMRI data from two large groups, researchers found an increase in inhibition in certain brain regions (association cortices) as adolescents age, while sensorimotor areas showed more stable excitation levels.
  • - The findings suggest that there’s a consistent developmental pattern in the excitation-inhibition balance that can vary among individuals, providing a new computational method to study brain maturation at a personal level.
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Background: Personality traits have been associated with eating disorders (EDs) and comorbidities. However, it is unclear which personality profiles are premorbid risk rather than diagnostic markers.

Methods: We explored associations between personality and ED-related mental health symptoms using canonical correlation analyses.

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Current psychiatric diagnoses are not defined by neurobiological measures which hinders the development of therapies targeting mechanisms underlying mental illness . Research confined to diagnostic boundaries yields heterogeneous biological results, whereas transdiagnostic studies often investigate individual symptoms in isolation. There is currently no paradigm available to comprehensively investigate the relationship between different clinical symptoms, individual disorders, and the underlying neurobiological mechanisms.

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Background: Depressive symptoms are highly prevalent, present in heterogeneous symptom patterns, and share diverse neurobiological underpinnings. Understanding the links between psychopathological symptoms and biological factors is critical in elucidating its etiology and persistence. We aimed to evaluate the utility of using symptom-brain network models to parse the heterogeneity of depressive complaints in a large adolescent sample.

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Introduction: Rare copy number variants (CNVs) and polygenic risk for intelligence (PRS-IQ) both confer susceptibility for autism spectrum disorder (ASD) but have opposing effects on cognitive ability. The field has struggled to disentangle the effects of these two classes of genomic variants on cognitive ability from their effects on ASD susceptibility, in part because previous studies did not include controls with cognitive measures. We aim to investigate the impact of these genomic variants on ASD risk while adjusting for their known effects on cognitive ability.

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  • * Neuroimaging reveals that many of these genetic variants have widespread effects on brain regions and are linked to various cancers and specific signaling pathways, such as p53 and Wnt.
  • * The findings suggest a connection between the genes that regulate head size and the likelihood of cancer, emphasizing the need for further research on the implications of this relationship.
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Background: Alzheimer's disease (AD)-related neuropathological changes can occur decades before clinical symptoms. We aimed to investigate whether neurodevelopment and/or neurodegeneration affects the risk of AD, through reducing structural brain reserve and/or increasing brain atrophy, respectively.

Methods: We used bidirectional two-sample Mendelian randomisation to estimate the effects between genetic liability to AD and global and regional cortical thickness, estimated total intracranial volume, volume of subcortical structures and total white matter in 37 680 participants aged 8-81 years across 5 independent cohorts (Adolescent Brain Cognitive Development, Generation R, IMAGEN, Avon Longitudinal Study of Parents and Children and UK Biobank).

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Obesity is a major modifiable risk factor for Alzheimer's disease (AD), characterized by progressive atrophy of the cerebral cortex. The neurobiology of obesity contributions to AD is poorly understood. Here we show with in vivo MRI that diet-induced obesity decreases cortical volume in mice, and that higher body adiposity associates with lower cortical volume in humans.

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