{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,30]],"date-time":"2026-10-30T21:27:57Z","timestamp":1793395677603,"version":"4.5.0"},"reference-count":185,"publisher":"MDPI AG","issue":"18","license":[{"start":{"date-parts":[[2024,9,11]],"date-time":"2024-09-11T00:00:00Z","timestamp":1726012800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["IJMS"],"abstract":"<jats:p>Understanding the molecular mechanisms underlying the generation of absence seizures is crucial for developing effective, patient-specific treatments for childhood absence epilepsy (CAE). Currently, one-third of patients remain refractive to the antiseizure medications (ASMs), previously called antiepileptic drugs (AEDs), available to treat CAE. Additionally, these ASMs often produce serious side effects and can even exacerbate symptoms in some patients. Determining the precise cellular and molecular mechanisms directly responsible for causing this type of epilepsy has proven challenging as they appear to be complex and multifactorial in patients with different genetic backgrounds. Aberrant neuronal activity in CAE may be caused by several mechanisms that are not fully understood. Thus, dissecting the causal factors that could be targeted in the development of precision medicines without side effects remains a high priority and the ultimate goal in this field of epilepsy research. The aim of this review is to highlight our current understanding of potential causative mechanisms for absence seizure generation, based on the latest research using cutting-edge technologies. This information will be important for identifying potential targets for future therapeutic intervention.<\/jats:p>","DOI":"10.3390\/ijms25189821","type":"journal-article","created":{"date-parts":[[2024,9,11]],"date-time":"2024-09-11T05:45:12Z","timestamp":1726033512000},"page":"9821","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":12,"title":["Molecular Mechanisms Underlying the Generation of Absence Seizures: Identification of Potential Targets for Therapeutic Intervention"],"prefix":"10.3390","volume":"25","author":[{"given":"Beulah","family":"Leitch","sequence":"first","affiliation":[{"name":"Department of Anatomy, School of Biomedical Sciences, Brain Health Research Centre, University of Otago, Dunedin 9054, New Zealand"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1968","published-online":{"date-parts":[[2024,9,11]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","first-page":"689","DOI":"10.1016\/S0140-6736(18)32596-0","article-title":"Epilepsy in adults","volume":"393","author":"Thijs","year":"2019","journal-title":"Lancet"},{"key":"ref_2","doi-asserted-by":"crossref","first-page":"23","DOI":"10.1212\/WNL.0b013e318204a36a","article-title":"Estimating risk for developing epilepsy","volume":"76","author":"Hesdorffer","year":"2011","journal-title":"Neurology"},{"key":"ref_3","doi-asserted-by":"crossref","first-page":"459","DOI":"10.1016\/S1474-4422(18)30499-X","article-title":"Global, regional, and national burden of neurological disorders, 1990\u20132016: A systematic analysis for the Global Burden of Disease Study 2016","volume":"18","author":"Feigin","year":"2019","journal-title":"Lancet Neurol."},{"key":"ref_4","doi-asserted-by":"crossref","first-page":"475","DOI":"10.1111\/epi.12550","article-title":"ILAE Official Report: A practical clinical definition of epilepsy","volume":"55","author":"Fisher","year":"2014","journal-title":"Epilepsia"},{"key":"ref_5","doi-asserted-by":"crossref","first-page":"522","DOI":"10.1111\/epi.13670","article-title":"Operational classification of seizure types by the International League Against Epilepsy: Position Paper of the ILAE Commission for Classification and Terminology","volume":"58","author":"Fisher","year":"2017","journal-title":"Epilepsia"},{"key":"ref_6","doi-asserted-by":"crossref","first-page":"531","DOI":"10.1111\/epi.13671","article-title":"Instruction manual for the ILAE 2017 operational classification of seizure types","volume":"58","author":"Fisher","year":"2017","journal-title":"Epilepsia"},{"key":"ref_7","doi-asserted-by":"crossref","first-page":"512","DOI":"10.1111\/epi.13709","article-title":"ILAE classification of the epilepsies: Position paper of the ILAE Commission for Classification and Terminology","volume":"58","author":"Scheffer","year":"2017","journal-title":"Epilepsia"},{"key":"ref_8","doi-asserted-by":"crossref","first-page":"1475","DOI":"10.1111\/epi.17236","article-title":"ILAE definition of the Idiopathic Generalized Epilepsy Syndromes: Position statement by the ILAE Task Force on Nosology and Definitions","volume":"63","author":"Hirsch","year":"2022","journal-title":"Epilepsia"},{"key":"ref_9","doi-asserted-by":"crossref","first-page":"523","DOI":"10.1111\/epi.13996","article-title":"Generalized nonmotor (absence) seizuresWhat do absence, generalized, and nonmotor mean?","volume":"59","author":"Unterberger","year":"2018","journal-title":"Epilepsia"},{"key":"ref_10","doi-asserted-by":"crossref","first-page":"56","DOI":"10.1007\/s10309-022-00469-w","article-title":"Generalized absence seizures: Where do we stand today?","volume":"35","author":"Stefan","year":"2022","journal-title":"Z. 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