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In Sweden, the prevalence of AE varies considerably between regions, suggesting underdiagnosis. We hypothesized that some undetected AE patients would attend Swedish memory clinics.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      We retrospectively screened 1021 individuals attending the Karolinska University Hospital memory clinics for AE autoantibodies. Serum screening was performed with live cell-based assays (CBAs) for antibodies to contactin-associated protein-like 2 (CASPR2), gamma-aminobutyric acid receptor B (GABA\n                      <jats:sub>B<\/jats:sub>\n                      R), immunoglobulin superfamily containing LAMP, OBCAM, and neurotrimin family member 5 (IgLON5), leucine-rich glioma-inactivated 1 (LGI1), and n-methyl-d-aspartate receptor (NMDA-R). Positive serum and CSF samples were further tested with fixed CBAs and tissue-based assays.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Eleven patients were antibody-positive in two or more independent tests. When investigating clinical information, three patients had phenotypes suggesting paraneoplastic (PE) or autoimmune encephalitis. These patients had antibodies to either CASPR2 or NMDA-R in serum and CSF and either had CSF-specific electrophoresis IgG-bands or increased Kappa free light-chain-intrathecal fraction. In four patients, available clinical information was insufficient to clarify if the antibodies were related to an ongoing or past encephalitis or lacked relevance, with a\u00a0further three considered false positive. The final individual had previously been diagnosed with LGI1-AE. When the STAM3mP score, a tool for identifying treatment-responsive rapidly progressive dementia, was used on the seven previously undiagnosed patients with antibodies of possible relevance, six got one point, indicating potential treatment response.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>AE is a rare differential diagnosis in our study of memory clinic visitors. Given the low prevalence, we conclude that AE autoantibody testing is not suitable for unselective screening in this setting. Instead, a rigorous clinical evaluation, potentially supported by tools like the STAM3mP score, might acceptably limit the number of missed AE cases among patients suffering from memory impairment, but further studies on pre-screening biomarkers are warranted.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1007\/s00415-026-13953-4","type":"journal-article","created":{"date-parts":[[2026,6,20]],"date-time":"2026-06-20T10:57:42Z","timestamp":1781953062000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Screening 1021 Swedish memory clinic visitors for autoantibody-mediated encephalitis"],"prefix":"10.1007","volume":"273","author":[{"given":"A.","family":"Freitas-Huhtam\u00e4ki","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"N.","family":"Kleebauer","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"A.","family":"Gardner","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J.","family":"Lundberg","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"M.","family":"Esbj\u00f6rnsson","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"R.","family":"Da Silva Rodrigues","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"P.","family":"Waters","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"M.","family":"Scheller-Nissen","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"M.","family":"Blaabjerg","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"N.","family":"Bogdanovic","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8752-3151","authenticated-orcid":false,"given":"J.","family":"Theorell","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2026,6,20]]},"reference":[{"key":"13953_CR1","doi-asserted-by":"publisher","DOI":"10.1016\/j.neuropharm.2017.04.046","author":"J Varley","year":"2017","unstructured":"Varley J, Taylor J, Irani SR (2017) Autoantibody-mediated diseases of the CNS: structure, dysfunction and therapy. 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He has not received any research grants, restricted, or unrestricted, for this or any other work. PW is a named inventor on patents for antibody assays (WO\/2010\/046716) with royalties paid by Euroimmun AG and disease biomarker patents (WO2019211633A1, WO2022189788A1). He has received honoraria from Biogen Idec, Mereo Biopharma, Retrogenix, UBC, Euroimmun AG, UCB, F. Hoffmann La-Roche, Forum for Indian Neurology Education (FINE) and Alexion; and research funding from Euroimmun AG. He serves on the editorial boards of Neurology, Neuroimmunology & Neuroinflammation and the Journal of Clinical Neurology. Antibody testing for patient care in the UK is carried out in the Oxford Autoimmune Neurology Diagnostic Laboratory. No other authors report any potential conflicts of interest.","order":2,"name":"Ethics","group":{"name":"EthicsHeading","label":"Conflicts of interest"}},{"value":"This study was approved by the Swedish Ethical Review Authority, registration number 2011\/1987\u201331 and 2022\/03556\u201301. Patients who were able to do so provided written consent after receiving oral and written information about the study. For patients who could not comprehend the information due to severe cognitive decline, written informed consent was provided by their legal guardian or next of kin. This procedure was in accordance with the rules set by the Swedish Ethical Review Authority for the project.","order":3,"name":"Ethics","group":{"name":"EthicsHeading","label":"Ethical approval"}},{"value":"Patients who were able to do so provided written consent after receiving oral and written information about the study. For patients who could not comprehend the information due to severe cognitive decline, written informed consent was provided by their legal guardian or next of kin.","order":4,"name":"Ethics","group":{"name":"EthicsHeading","label":"Informed consent"}}],"article-number":"408"}}