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  3. Associations between epilepsy-related polygenic risk and brain morphology in childhood.

Associations between epilepsy-related polygenic risk and brain morphology in childhood.

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DOI
10.48620/90841
Publisher DOI
10.1093/brain/awaf259
PubMed ID
40811581
Abstract
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 individuals We 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.
Date Issued
2026-02-07
Publication Type
Article
Subject(s)
600 Technology > 610 Medicine & health
Subjects
brain structure
•
childhood
•
genetic risk
•
imaging-genetics
•
temporal lobe epilepsy
Language(s)
en
Author(s)
Ngo, Alexander
Liu, Lang
Larivière, Sara
Kebets, Valeria
Fett, Serena
Weber, Clara F
Royer, Jessica
Yu, Eric
Rodríguez-Cruces, Raúl
Zhang, Zhiqiang
Ooi, Leon Qi Rong
Yeo, B T Thomas
Frauscher, Birgit
Paquola, Casey
Caligiuri, Maria Eugenia
Gambardella, Antonio
Concha, Luis
Keller, Simon S
Cendes, Fernando
Yasuda, Clarissa L
Bonilha, Leonardo
Gleichgerrcht, Ezequiel
Focke, Niels K
Kotikalapudi, Raviteja  
O'Brien, Terence J
Sinclair, Benjamin
Vivash, Lucy
Desmond, Patricia M
Lui, Elaine
Vaudano, Anna Elisabetta
Meletti, Stefano
Kälviäinen, Reetta
Soltanian-Zadeh, Hamid
Winston, Gavin P
Tiwari, Vijay K
Kreilkamp, Barbara A K
Lenge, Matteo
Guerrini, Renzo
Hamandi, Khalid
Rüber, Theodor
Bauer, Tobias
Devinsky, Orrin
Striano, Pasquale
Kaestner, Erik
Hatton, Sean N
Caciagli, Lorenzo  
Clinic of Neurology  
Kirschner, Matthias
Duncan, John S
Thompson, Paul M
McDonald, Carrie R
Sisodiya, Sanjay M
Bernasconi, Neda
Bernasconi, Andrea
Gan-Or, Ziv
Bernhardt, Boris C
Additional Credits
Clinic of Neurology  
Journal
Brain
Publisher
Oxford University Press
ISSN
1460-2156
0006-8950
Access(Rights)
open.access
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