<HashMap><database>GEO</database><file_versions><headers><Content-Type>application/xml</Content-Type></headers><body><files><Other>ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE303nnn/GSE303810/</Other></files><type>primary</type></body><statusCode>OK</statusCode><statusCodeValue>200</statusCodeValue></file_versions><scores/><additional><omics_type>Transcriptomics</omics_type><species>Homo sapiens</species><gds_type>Expression profiling by high throughput sequencing</gds_type><full_dataset_link>https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE303810</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>snRNA-seq profiles distinguish anti-Drebrin- and anti-GAD65-positive encephalitis</name><description>Autoantibodies (ABs) against intracellular proteins, including glutamate-decarboxylase 65 (anti-GAD65), are increasingly recognized in autoimmune and limbic encephalitis (AE/LE). Anti-GAD65 LE frequently progresses into severe temporal lobe epilepsy (TLE), neuropathologically characterized by hippocampal sclerosis (HS) and variable cytotoxic T lymphocytes (CTLs) infiltration. Recently, we have identified Drebrin as a novel intracellular target protein of ABs in patients suspicious for AE. Here, we report on the hippocampal neuropathological sequelae and single-nuclei RNA sequencing (snRNA-seq) of anti-Drebrin- versus anti-GAD65-positive TLE patients, in concert with key clinical parameters from a large patient cohort.</description><dates><publication>2026/07/09</publication></dates><accession>GSE303810</accession><cross_references><GSM>GSM9136272</GSM><GSM>GSM9136271</GSM><GSM>GSM9136274</GSM><GSM>GSM9136273</GSM><GSM>GSM9136276</GSM><GSM>GSM9136275</GSM><GSM>GSM9136277</GSM><GSM>GSM9136270</GSM><GPL>24676</GPL><GSE>303810</GSE><taxon>Homo sapiens</taxon><PMID>[42415095]</PMID></cross_references></HashMap>