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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 individuals.<\/jats:p>\n                  <jats:p>We used genome-wide genotyping and structural T1-weighted MRI of 3826 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 1512 healthy controls aggregated across multiple sites.<\/jats:p>\n                  <jats:p>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 were highly replicable across different studies. Findings were consistent when using statistical models controlling for spatial autocorrelations and robust to variations in analytic methods.<\/jats:p>\n                  <jats:p>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.<\/jats:p>","DOI":"10.1093\/brain\/awaf259","type":"journal-article","created":{"date-parts":[[2025,8,8]],"date-time":"2025-08-08T12:11:05Z","timestamp":1754655065000},"page":"519-533","source":"Crossref","is-referenced-by-count":3,"title":["Associations between epilepsy-related polygenic risk and brain morphology in childhood"],"prefix":"10.1093","volume":"149","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-8999-9388","authenticated-orcid":false,"given":"Alexander","family":"Ngo","sequence":"first","affiliation":[{"name":"Montreal Neurological Institute and Hospital, McGill University , Montreal, QC , H3A 2B4","place":["Canada"]},{"name":"Department of Neurology and Neurosurgery, McGill University , Montreal, QC , H3A 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