Evidence map›Paper›PMID 42322434›Full record

ArticleJournal of neurology2026

Screening 1021 Swedish memory clinic visitors for autoantibody-mediated encephalitis.

A Freitas-Huhtamäki, N Kleebauer, A Gardner, J Lundberg, M Esbjörnsson, R Da Silva Rodrigues, P Waters, M Scheller-Nissen, M Blaabjerg, N Bogdanovic and 1 more

Abstract read
In one paragraph

Article in Journal of neurology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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1 · What the graph read from it

What it found

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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

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Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

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PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors.

A Freitas-HuhtamäkiCenter for Infectious Medicine, Department of Medicine Huddinge, Karolinska Institutet, CIM/ANA Futura, Alfred Nobles Allé 8B, 141 52, Stockholm, Sweden.
N KleebauerCenter for Infectious Medicine, Department of Medicine Huddinge, Karolinska Institutet, CIM/ANA Futura, Alfred Nobles Allé 8B, 141 52, Stockholm, Sweden.
A GardnerCenter for Infectious Medicine, Department of Medicine Huddinge, Karolinska Institutet, CIM/ANA Futura, Alfred Nobles Allé 8B, 141 52, Stockholm, Sweden.
J LundbergMedical unit of Geriatric Medicine, Theme Inflammation and Aging, Karolinska University Hospital, Stockholm, Sweden.
M EsbjörnssonDepartment of Clinical Sciences, University of Lund, Lund, Sweden.
R Da Silva RodriguesMedical Unit of Clinical Immunology and Transfusion Medicine, Function Medical Diagnostics, Karolinska University Hospital, Stockholm, Sweden.
P WatersNuffield Department of Clinical Neurosciences, University of Oxford, Oxford, UK.
M Scheller-NissenDepartment of Clinical Medicine, University of Southern Denmark, Odense, Denmark.
M BlaabjergDepartment of Clinical Medicine, University of Southern Denmark, Odense, Denmark.
N BogdanovicMedical unit of Geriatric Medicine, Theme Inflammation and Aging, Karolinska University Hospital, Stockholm, Sweden.
J TheorellCenter for Infectious Medicine, Department of Medicine Huddinge, Karolinska Institutet, CIM/ANA Futura, Alfred Nobles Allé 8B, 141 52, Stockholm, Sweden. Jakob.theorell@ki.se.ORCID http://orcid.org/0000-0001-8752-3151

Funding

Alzheimerfonden AF-981112Svenska Läkaresällskapet SLS-974288Wenner-Gren Stiftelserna FT2021-0005Wenner-Gren Stiftelserna WUP2022-003
6 · The paper itself

Abstract

introductionA treatable differential diagnosis to neurodegenerative dementia is autoimmune encephalitis (AE). In Sweden, the prevalence of AE varies considerably between regions, suggesting underdiagnosis. We hypothesized that some undetected AE patients would attend Swedish memory clinics.

methodsWe 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

resultsEleven 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 further 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.

conclusionAE 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.

Indexed as

AutoantibodiesAutoimmune Diseases of the Nervous SystemEncephalitisHashimoto DiseaseAdultAgedAged, 80 and overFemaleHumansIntracellular Signaling Peptides and ProteinsMaleMembrane ProteinsMiddle AgedNerve Tissue ProteinsReceptors, N-Methyl-D-AspartateRetrospective StudiesAutoantibodiesCNTNAP2 protein, humanIntracellular Signaling Peptides and ProteinsLGI1 protein, humanMembrane ProteinsNerve Tissue ProteinsReceptors, N-Methyl-D-AspartateAutoantibody detectionAutoimmune encephalitisNeurodegenerative dementiaNeuroimmunologyScreening

Identifiers

PMID42322434
PMCPMC13283170

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.