{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,28]],"date-time":"2026-08-28T07:18:59Z","timestamp":1787901539265,"version":"build-2784847793"},"reference-count":35,"publisher":"Wiley","issue":"8","license":[{"start":{"date-parts":[[2026,7,29]],"date-time":"2026-07-29T00:00:00Z","timestamp":1785283200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,7,29]],"date-time":"2026-07-29T00:00:00Z","timestamp":1785283200000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/501100004735","name":"Natural Science Foundation of Hunan Province","doi-asserted-by":"publisher","award":["2025JJ60695"],"award-info":[{"award-number":["2025JJ60695"]}],"id":[{"id":"10.13039\/501100004735","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["82471488"],"award-info":[{"award-number":["82471488"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["CNS Neurosci Ther"],"published-print":{"date-parts":[[2026,8]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Aim<\/jats:title>\n                    <jats:p>To describe the genotypic and phenotypic profile of chromatin remodeling complex (CRC)\u2010related neurological disorders.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>We retrospectively analyzed the clinical characteristics and the genetic spectrum of children with variants in CRC genes.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Fifty patients were included. The genotype spectrum involved genes encoding the CHD complex (\n                      <jats:italic>CHD2<\/jats:italic>\n                      ,\n                      <jats:italic>CHD3<\/jats:italic>\n                      ,\n                      <jats:italic>CHD4<\/jats:italic>\n                      ,\n                      <jats:italic>CHD7<\/jats:italic>\n                      ,\n                      <jats:italic>CHD8<\/jats:italic>\n                      ), the BAF complex (\n                      <jats:italic>SMARCA2<\/jats:italic>\n                      ,\n                      <jats:italic>ARID1B<\/jats:italic>\n                      ,\n                      <jats:italic>ARID2<\/jats:italic>\n                      ,\n                      <jats:italic>ACTB<\/jats:italic>\n                      ), and the ISWI complex (\n                      <jats:italic>BPTF<\/jats:italic>\n                      ). The predominant phenotypes were global developmental delay\/intellectual disability (GDD\/ID) (76.0%, 38\/50) and epilepsy (64.0%, 32\/50). Seventy\u2010five percent of patients with epilepsy had generalized seizures. Sixty\u2010nine percent (20\/29) were seizure\u2010free for more than 1\u2009year at the last follow\u2010up (three were lost to follow\u2010up), although 56.3% (18\/32) of patients required three or more kinds of antiseizure medications. EEG abnormalities were prevalent (82.2%, 37\/45), commonly showing generalized or diffuse interictal discharges (63.6%), slow background activity (59.5%), and slow waves (35.1%). BAF complex variants were significantly associated with GDD\/ID, microcephaly, facial dysmorphism, short stature, and slow background activity on EEG, while CHD complex variants were more likely to cause heat\u2010sensitive seizures (FDR\u2009&lt;\u20090.05).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>\n                      CRC\u2010related disorders are primarily caused by variants in the CHD and BAF complexes, with\n                      <jats:italic>CHD2<\/jats:italic>\n                      ,\n                      <jats:italic>ARID1B<\/jats:italic>\n                      , and\n                      <jats:italic>SMARCA2<\/jats:italic>\n                      being the frequently involved genes. The conditions are characterized by GDD\/ID and epilepsy, with distinct clinical patterns between the CHD and BAF complexes.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/cns.71061","type":"journal-article","created":{"date-parts":[[2026,7,30]],"date-time":"2026-07-30T04:18:11Z","timestamp":1785385091000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Genotypic and Phenotypic Profile of 50 Cases With Chromatin Remodeling Complexes\u2010Related Neurological Disorders"],"prefix":"10.1002","volume":"32","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-5255-8992","authenticated-orcid":false,"given":"Shimeng","family":"Chen","sequence":"first","affiliation":[{"name":"Department of Pediatrics Xiangya Hospital of Central South University  Changsha China"},{"name":"Clinical Research Center for Children Neurodevelopmental Disabilities of Hunan Province  Changsha 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