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| Hauptseite > Online First > Associations between epilepsy-related polygenic risk and brain morphology in childhood > print |
| Hauptseite > Online First > Associations between epilepsy-related polygenic risk and brain morphology in childhood > print |
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| 005 | 20260121152242.0 | ||
| 024 | 7 | _ | |a 10.1093/brain/awaf259 |2 doi |
| 024 | 7 | _ | |a 0006-8950 |2 ISSN |
| 024 | 7 | _ | |a 1460-2156 |2 ISSN |
| 037 | _ | _ | |a FZJ-2026-00802 |
| 082 | _ | _ | |a 610 |
| 100 | 1 | _ | |a Ngo, Alexander |0 P:(DE-HGF)0 |b 0 |
| 245 | _ | _ | |a Associations between epilepsy-related polygenic risk and brain morphology in childhood |
| 260 | _ | _ | |a Oxford |c 2025 |b Oxford Univ. Press |
| 336 | 7 | _ | |a article |2 DRIVER |
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| 336 | 7 | _ | |a ARTICLE |2 BibTeX |
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| 336 | 7 | _ | |a Journal Article |0 0 |2 EndNote |
| 520 | _ | _ | |a Extensive neuroimaging research in temporal lobe epilepsy with hippocampal sclerosis (TLE-HS) has identified brain atrophy as a disease phenotype. While it is also related to a complex genetic architecture, the transition from genetic risk factors to brain vulnerabilities remains unclear. Using a population-based approach, we examined the associations between epilepsy-related polygenic risk for HS (PRS-HS) and brain structure in healthy developing children, assessed their relation to brain network architecture, and evaluated its correspondence with case-control findings in TLE-HS diagnosed patients relative to healthy individualsWe used genome-wide genotyping and structural T1-weighted magnetic resonance imaging (MRI) of 3,826 neurotypical children from the Adolescent Brain Cognitive Development (ABCD) study. Surface-based linear models related PRS-HS to cortical thickness measures, and subsequently contextualized findings with structural and functional network architecture based on epicentre mapping approaches. Imaging-genetic associations were then correlated to atrophy and disease epicentres in 785 patients with TLE-HS relative to 1,512 healthy controls aggregated across multiple sites.Higher PRS-HS was associated with decreases in cortical thickness across temporo-parietal as well as fronto-central regions of neurotypical children. These imaging-genetic effects were anchored to the connectivity profiles of distinct functional and structural epicentres. Compared with disease-related alterations from a separate epilepsy cohort, regional and network correlates of PRS-HS strongly mirrored cortical atrophy and disease epicentres observed in patients with TLE-HS, and highly replicable across different studies. Findings were consistent when using statistical models controlling for spatial autocorrelations and robust to variations in analytic methods.Capitalizing on recent imaging-genetic initiatives, our study provides novel insights into the genetic underpinnings of structural alterations in TLE-HS, revealing common morphological and network pathways between genetic vulnerability and disease mechanisms. These signatures offer a foundation for early risk stratification and personalized interventions targeting genetic profiles in epilepsy. |
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| 773 | _ | _ | |a 10.1093/brain/awaf259 |g p. awaf259 |0 PERI:(DE-600)1474117-9 |p awaf259 |t Brain |v . |y 2025 |x 0006-8950 |
| 856 | 4 | _ | |u https://academic.oup.com/brain/advance-article/doi/10.1093/brain/awaf259/8234529?login=true#supplementary-data |
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