{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,20]],"date-time":"2026-10-20T04:38:53Z","timestamp":1792471133070,"version":"4.5.0"},"reference-count":127,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2026,8,19]],"date-time":"2026-08-19T00:00:00Z","timestamp":1787097600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,8,19]],"date-time":"2026-08-19T00:00:00Z","timestamp":1787097600000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Epilepsia Open"],"published-print":{"date-parts":[[2026,10]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:label\/>\n                    <jats:p>Epilepsy comprises a highly heterogeneous group of neurological disorders unified by a persistent predisposition to recurrent seizures, yet driven by remarkably diverse genetic, molecular, and network\u2010level mechanisms. Advances in genomic technologies have revealed that epilepsy arises from a multilayered genetic architecture encompassing rare high\u2010penetrance monogenic variants, common polygenic risk factors, brain\u2010restricted somatic mosaicism, and extensive gene\u2013environment interactions. These genetic substrates converge on core biological pathways regulating neuronal excitability, synaptic transmission, metabolic homeostasis, neuroinflammation, and circuit development. In this review, we synthesize contemporary insights into the genetic and molecular pathophysiology of seizures and epilepsy, with emphasis on mechanisms that destabilize excitation\u2013inhibition balance, promote epileptogenesis, and drive pharmacoresistance. We highlight how ion channel dysfunction, synaptic vesicle cycling defects, mTOR pathway hyperactivation, glial and metabolic failure, and inflammatory cascades interact to lower seizure threshold and remodel neural networks. Beyond classical monogenic and polygenic models, we discuss the emerging role of somatic mutations, polygenic modifiers of rare variants, and dynamic brain\u2010state\u2013dependent seizure susceptibility. We further integrate genetic mechanisms with clinical heterogeneity, including age of onset, seizure type, penetrance, pleiotropy, and treatment response, and review translational implications for precision medicine, pharmacogenomics, and emerging molecular therapies such as antisense oligonucleotides, gene regulation strategies, and cell\u2010based interventions. Understanding the genetic architecture of epilepsy is increasingly informing diagnostic pathways, prognostic stratification, and the development of precision\u2010based therapeutic approaches.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Plain Language Summary<\/jats:title>\n                    <jats:p>Epilepsy genetics extends beyond single\u2010gene disorders and involves multiple interacting layers of genomic variation. In this review, we integrate evidence across rare variants, polygenic risk, somatic mosaicism, and genetic modifiers to provide a broader framework for understanding seizure susceptibility and clinical diversity. By highlighting convergent biological pathways and their effects on neuronal networks, this work supports more refined approaches to epilepsy classification and future precision medicine strategies.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/epi4.70310","type":"journal-article","created":{"date-parts":[[2026,8,19]],"date-time":"2026-08-19T10:51:46Z","timestamp":1787136706000},"page":"1395-1412","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["The genetic architecture of epilepsy across molecular mechanisms and clinical heterogeneity"],"prefix":"10.1002","volume":"11","author":[{"ORCID":"https:\/\/orcid.org\/0009-0003-1381-4580","authenticated-orcid":false,"given":"Mohammad Reza","family":"Seyedtaghia","sequence":"first","affiliation":[{"name":"Department of Medical Genetics, Faculty of Medicine Hormozgan University of Medical Sciences  Bandar Abbas 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