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Transl. Med."],"published-print":{"date-parts":[[2026,5,13]]},"abstract":"<jats:p>\n                    Dravet syndrome (DS) is a severe neurodevelopmental disorder characterized by drug-resistant epilepsy, temperature-sensitive seizures, cognitive impairment, and a high incidence of sudden unexpected death in epilepsy (SUDEP). DS is caused by loss-of-function variants in\n                    <jats:italic toggle=\"yes\">SCN1A<\/jats:italic>\n                    , which encodes the \u03b1 subunit of the voltage-gated sodium channel (Na\n                    <jats:sub>v<\/jats:sub>\n                    1.1). Current approved treatments manage symptoms of DS but do not correct the root cause of the disease. Here, we describe the use of an adenine base editor (ABE) to directly correct\n                    <jats:italic toggle=\"yes\">\n                      SCN1A\n                      <jats:sup>R613X<\/jats:sup>\n                    <\/jats:italic>\n                    , a recurrent variant found in patients with DS. We identified ABE strategies to efficiently correct R613X in engineered homozygous\n                    <jats:italic toggle=\"yes\">\n                      SCN1A\n                      <jats:sup>R613X<\/jats:sup>\n                    <\/jats:italic>\n                    human embryonic kidney 293T and mouse Neuro-2a cells (72 and 92% correction efficiencies, respectively). We then used a dual\u2013adeno-associated virus serotype 9 (AAV9) approach to deliver an optimized ABE system to\n                    <jats:italic toggle=\"yes\">\n                      Scn1a\n                      <jats:sup>R613X\/+<\/jats:sup>\n                    <\/jats:italic>\n                    mice, which recapitulate several key DS pathologies. AAV9-ABE treatment of\n                    <jats:italic toggle=\"yes\">\n                      Scn1a\n                      <jats:sup>R613X\/+<\/jats:sup>\n                    <\/jats:italic>\n                    neonates resulted in efficient DNA and mRNA editing (59 and 97%, respectively, in bulk neocortices), restoring parvalbumin-expressing inhibitory neuron excitability and sodium current to wild-type levels. This ameliorated both spontaneous and temperature-induced seizures and led to a 3.3-fold improvement in 45-day survival over vehicle-treated mice (ABE treated,\u00a090%; and vehicle treated, 27%). Last, ABE treatment in 12-day-old mice resulted in a 3.0-fold improvement in 60-day survival over vehicle-treated mice (ABE treated,\u00a082%; and vehicle treated, 27%). In conclusion, these data validate a strategy to correct\n                    <jats:italic toggle=\"yes\">SCN1A<\/jats:italic>\n                    variants with ABE and highlight the potential of precision genome editing treatments for the treatment of DS and possibly other neurodevelopmental disorders.\n                  <\/jats:p>","DOI":"10.1126\/scitranslmed.adx5999","type":"journal-article","created":{"date-parts":[[2026,5,13]],"date-time":"2026-05-13T17:58:22Z","timestamp":1778695102000},"update-policy":"https:\/\/doi.org\/10.34133\/aaas_crossmark","source":"Crossref","is-referenced-by-count":3,"title":["In vivo adenine base editing ameliorates Dravet syndrome phenotypes in a mouse model"],"prefix":"10.1126","volume":"18","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-2591-0428","authenticated-orcid":true,"given":"Andrew T.","family":"Nelson","sequence":"first","affiliation":[{"name":"Merkin Institute of Transformative Technologies in Healthcare, Broad Institute of Harvard 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USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-2896-3469","authenticated-orcid":true,"given":"J\u00e9r\u00f4me","family":"Clatot","sequence":"additional","affiliation":[{"name":"Division of Neurology, Department of Pediatrics, Children\u2019s Hospital of Philadelphia, Philadelphia, PA 19104, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9338-1484","authenticated-orcid":true,"given":"Holt A.","family":"Sakai","sequence":"additional","affiliation":[{"name":"Merkin Institute of Transformative Technologies in Healthcare, Broad Institute of Harvard and MIT, Cambridge, MA 02142, USA."},{"name":"Department of Chemistry and Chemical Biology, Harvard University, Cambridge, MA 02138, USA."},{"name":"Howard Hughes Medical Institute, Harvard University, Cambridge, MA 02138, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9565-1567","authenticated-orcid":true,"given":"Jun","family":"Xie","sequence":"additional","affiliation":[{"name":"Horae Gene Therapy Center, UMass Chan Medical School, University of Massachusetts, Worcester, MA 01655, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alexander A.","family":"Sousa","sequence":"additional","affiliation":[{"name":"Merkin Institute of Transformative Technologies in Healthcare, Broad Institute of Harvard and MIT, Cambridge, MA 02142, USA."},{"name":"Department of Chemistry and Chemical Biology, Harvard University, Cambridge, MA 02138, USA."},{"name":"Howard Hughes Medical Institute, Harvard University, Cambridge, MA 02138, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4006-8670","authenticated-orcid":true,"given":"Meirui","family":"An","sequence":"additional","affiliation":[{"name":"Merkin Institute of Transformative Technologies in Healthcare, Broad Institute of Harvard and MIT, Cambridge, MA 02142, USA."},{"name":"Department of Chemistry and Chemical Biology, Harvard University, Cambridge, MA 02138, USA."},{"name":"Howard Hughes Medical Institute, Harvard University, Cambridge, MA 02138, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0097-9012","authenticated-orcid":true,"given":"Guangping","family":"Gao","sequence":"additional","affiliation":[{"name":"Horae Gene Therapy Center, UMass Chan Medical School, University of Massachusetts, Worcester, MA 01655, USA."},{"name":"Microbiology and Physiological Systems, UMass Chan Medical School, University of Massachusetts, Worcester, MA 01655, 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