{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T13:57:35Z","timestamp":1791295055588,"version":"4.1.0"},"reference-count":50,"publisher":"Wiley","license":[{"start":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T00:00:00Z","timestamp":1791244800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T00:00:00Z","timestamp":1791244800000},"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":["Annals of Neurology"],"abstract":"<jats:sec>\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>\n                      To characterize regional brain atrophy patterns, evaluate their association with regional leucine\u2010rich glioma\u2010inactivated\u20101 (\n                      <jats:italic>LGI1<\/jats:italic>\n                      ) gene expression, and identify clinical predictors of hippocampal atrophy in LGI1 autoimmune encephalitis (AE).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      This study compared regional brain volumes in LGI1\u2010AE patients versus age\u2010 and sex\u2010matched healthy controls (HC) and Alzheimer's disease (AD) patients.\n                      <jats:italic>LGI1<\/jats:italic>\n                      gene expression was derived from the Allen Human Brain Atlas. Multivariable linear regression and generalized linear models were utilized.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      A total of 55 LGI1\u2010AE patients were included. Median age was 68\u2009years (IQR 62.5\u201374.2\u2009years) at volumetric analysis, after 19\u2009months (IQR 11\u201345\u2009months) from symptom onset. Compared with HC (\n                      <jats:italic>n<\/jats:italic>\n                      \u2009=\u200955) and AD patients (\n                      <jats:italic>n<\/jats:italic>\n                      \u2009=\u200955), LGI1\u2010AE patients had greater regional atrophy of the hippocampus, insula, caudate, and putamen (\n                      <jats:italic>p<\/jats:italic>\n                      \u2009&lt;\u20090.002). Longitudinal analyses demonstrated hippocampal and pallidal atrophy after covariate adjustment. Among those who did not fulfill limbic encephalitis criteria and\/or had non\u2010lesional magnetic resonance imaging, limbic and striatal atrophy were identified compared with HC (\n                      <jats:italic>p<\/jats:italic>\n                      \u2009&lt;\u20090.01). Regions with the greatest differential atrophy corresponded to higher\n                      <jats:italic>LGI1<\/jats:italic>\n                      gene expression (Spearman\n                      <jats:italic>\u03c1<\/jats:italic>\n                      \u2009=\u20090.7,\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.005). Severe cognitive deficits at diagnosis (\n                      <jats:italic>\u03b2<\/jats:italic>\n                      \u2009=\u2009\u22120.56;\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.002) and longer disease duration (\n                      <jats:italic>\u03b2<\/jats:italic>\n                      \u2009=\u2009\u22120.01;\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.001) independently predicted total hippocampal volume (\n                      <jats:italic>R<\/jats:italic>\n                      <jats:sup>2<\/jats:sup>\n                      \u2009=\u20090.31).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Interpretation<\/jats:title>\n                    <jats:p>\n                      LGI1\u2010AE demonstrates a distinct pattern of limbic and striatal atrophy that differs from AD and aligns with regional\n                      <jats:italic>LGI1<\/jats:italic>\n                      expression, supporting a model of selective network vulnerability. Greater baseline cognitive impairment and longer disease duration independently associated with hippocampal atrophy, underscoring the potential importance of early diagnosis and treatment to limit structural brain injury. ANN NEUROL 2026\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/ana.78389","type":"journal-article","created":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T13:08:22Z","timestamp":1791292102000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Selective Limbic and Striatal Atrophy Corresponds to Regional Gene Expression in Leucine\u2010Rich Glioma\u2010Inactivated\u20101\n                    <scp>Immunoglobulin\u2009G<\/scp>\n                    Autoimmune Encephalitis"],"prefix":"10.1002","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-5053-8544","authenticated-orcid":false,"given":"Albert","family":"Aboseif","sequence":"first","affiliation":[{"name":"Division of Multiple Sclerosis &amp; Autoimmune Neurology, Department of Neurology Mayo Clinic  Rochester MN USA"},{"name":"Center for Multiple Sclerosis &amp; Autoimmune Neurology Mayo Clinic  Rochester MN 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