{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,8]],"date-time":"2026-06-08T10:11:33Z","timestamp":1780913493198,"version":"3.54.1"},"reference-count":71,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2026,4,24]],"date-time":"2026-04-24T00:00:00Z","timestamp":1776988800000},"content-version":"vor","delay-in-days":23,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,4,1]],"date-time":"2026-04-01T00:00:00Z","timestamp":1775001600000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/501100005230","name":"Natural Science Foundation of Chongqing Municipality","doi-asserted-by":"publisher","award":["CSTB2023NSCQ\u2010MSX0216"],"award-info":[{"award-number":["CSTB2023NSCQ\u2010MSX0216"]}],"id":[{"id":"10.13039\/501100005230","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":[[2026,4]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Aims<\/jats:title>\n                    <jats:p>This study aims to investigate the underlying mechanisms of abnormal expression of \u03b1\u2010synuclein (\u03b1\u2010syn) in cortical lesions of focal cortical dysplasia IIb (FCD IIb) and tuberous sclerosis complex (TSC).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Cortical lesions of patients with FCD IIb and TSC were obtained during the surgery, FCD rats were generated by in utero X\u2010ray radiation. Immunostaining, RT\u2013PCR, Western blotting, and electroencephalography recording were conducted in this study. \u03b1\u2010syn was intraventricularly injected; mTOR inhibitor (rapamycin) and glutamate transporter\u20101 (GLT\u20101) enhancer (ceftriaxone sodium) were intraperitoneally injected before the following experiments.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>mTOR and p\u2010mTOR expressed in the dysmorphic neurons, vimentin\u2010positive balloon cells, and giant cells, whereas the mTOR\/p\u2010mTOR ratio was decreased in FCD IIb and TSC lesions. \u03b1\u2010syn was decreased, while p\u2010\u03b1\u2010syn was increased in the cortex of FCD animals, whereas they were rescued by inhibition of mTOR with rapamycin. The expression of GLT\u20101 was decreased and modulated by rapamycin in FCD animals. Enhancement of the function of GLT\u20101 with ceftriaxone ameliorated \u03b1\u2010synucleinopathy and seizure activities in FCD animals. Additionally, intracerebroventricular injection of \u03b1\u2010syn exerted anti\u2010seizure effects.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Our results showed that modulation of the mTOR\/GLT\u20101 pathway ameliorated \u03b1\u2010synucleinopathy and seizure activities in FCD, providing insights for understanding the epileptogenic mechanisms of FCD IIb and TSC.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/cns.70893","type":"journal-article","created":{"date-parts":[[2026,4,24]],"date-time":"2026-04-24T15:17:53Z","timestamp":1777043873000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["The Mechanism Underlying the Abnormal Expression of \u03b1\u2010Synuclein in the Cortical Lesions of Patients With\n                    <scp>FCD<\/scp>\n                    Type\n                    <scp>IIb<\/scp>\n                    and\n                    <scp>TSC<\/scp>"],"prefix":"10.1002","volume":"32","author":[{"ORCID":"https:\/\/orcid.org\/0009-0002-6596-5009","authenticated-orcid":false,"given":"Li","family":"Zhang","sequence":"first","affiliation":[{"name":"Department of Neurosurgery Epilepsy Research Center of PLA, Xinqiao Hospital, Army Medical University  Chongqing China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jian\u2010Ping","family":"Song","sequence":"additional","affiliation":[{"name":"Department of Neurosurgery Epilepsy Research Center of PLA, Xinqiao Hospital, Army Medical University  Chongqing China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jun","family":"Huang","sequence":"additional","affiliation":[{"name":"Department of Neurosurgery Epilepsy Research Center of PLA, Xinqiao Hospital, Army Medical University  Chongqing China"},{"name":"Chongqing Institute for Brain and Intelligence, Guang Yang Bay Laboratory  Chongqing China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ping","family":"Liang","sequence":"additional","affiliation":[{"name":"Department of Neurosurgery Children's Hospital of Chongqing Medical University, National Clinical Research Center for Child Health and Disorders, Ministry of Education Key Laboratory of Child Development and Disorders, Chongqing Key Laboratory of Pediatrics  Chongqing China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hui","family":"Yang","sequence":"additional","affiliation":[{"name":"Department of Neurosurgery Epilepsy Research Center of PLA, Xinqiao Hospital, Army Medical University  Chongqing China"},{"name":"Chongqing Institute for Brain and Intelligence, Guang Yang Bay Laboratory  Chongqing China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chun\u2010Qing","family":"Zhang","sequence":"additional","affiliation":[{"name":"Department of Neurosurgery Epilepsy Research Center of PLA, Xinqiao 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