Association of Brain Structural Measurements and Polygenic Risk Scores with Obsessive-Compulsive Symptoms in Adolescents Diagnosed with Obsessive-Compulsive Disorder, Attention-Deficit/Hyperactivity Disorder, Anxiety, Depression, Autism and Tic Disorders
Bibliographic record
Abstract
Obsessive-compulsive symptoms, characterized by intrusive thoughts and repetitive behaviors, are prevalent among youth. These symptoms are known to be moderately heritable and linked to structural brain changes involved in their pathophysiology. This study investigates the connections between structural brain alterations (cortical thickness, surface area and subcortical volume), genetic variation, and childhood obsessive-compulsive symptom scores within 143 samples of healthy control participants and cases diagnosed with obsessive-compulsive disorder, attention-deficit/hyperactivity disorder, anxiety disorder, autism spectrum disorders and/or tic disorders. We hypothesize that the effect of genetic variants on standardized scores of obsessive-compulsive symptoms is mediated by imaging endophenotypes. To do so we test for associations between polygenic risk scores and structural imaging phenotypes within cortico-striato-thalamo-cortical circuitry and perform mendelian randomization analyses to identify potential causal pathways linking polygenic risk scores of structural brain alterations and obsessive-compulsive symptoms assessed with the Obsessive-Compulsive Subscale of the Child Behavior Checklist. We observed that changes in cortical thickness of rostral middle frontal cortex and surface area of orbitofrontal cortex, along with other four regions have a significant genetic contribution in obsessive-compulsive symptom severity in adolescent samples. Additionally, surface area of inferior parietal lobule may act as a causal mediator between high-risk variants and obsessive-compulsive symptoms. The mentioned three regions are part of cortico-striato-thalamo-cortical circuitry that have various regulatory effects on obsessive-compulsive symptoms. If these findings replicated in larger samples, they could offer valuable insights into the neurobiology of obsessive-compulsive traits and related structural alterations in specific brain regions.
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How this classification was reachedexpand
Full frame distilled prediction
Teacher imitationNot calibrated prevalence, not ground truth. Human validation pending. Learned from the 10,348 direct Codex labels and 10,348 direct Gemma labels. Candidate is the union of thresholded teacher heads; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels or direct frontier model labels.
Codex and Gemma teacher scores by category
| Category | Codex | Gemma |
|---|---|---|
| Metaresearch | 0.000 | 0.001 |
| Meta-epidemiology (narrow) | 0.001 | 0.001 |
| Meta-epidemiology (broad) | 0.001 | 0.000 |
| Bibliometrics | 0.001 | 0.001 |
| Science and technology studies | 0.001 | 0.001 |
| Scholarly communication | 0.000 | 0.001 |
| Open science | 0.001 | 0.000 |
| Research integrity | 0.000 | 0.001 |
| Insufficient payload (model declined to judge) | 0.000 | 0.000 |
Machine scores (provisional)
The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.
Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.
score_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from itClassification
machine, unvalidatedMachine predicted; a candidate call from one teacher head, not a consensus.
How this classification was reached, model by model and score by score, is at the end of the page under "How this classification was reached".