Evidence map›Paper›PMID 42155449›Full record

ArticleCell reports. Medicine2026

Synaptophysin autoantibodies mediate synaptic dysfunction in cerebellar ataxia.

Samantha Ho, Hoi Kiu Wong, Dorina Shqau, Stephan Winklmeier, Marcus Grobe-Einsler, Kevin Rostasy, Tania Kümpfel, Franziska S Thaler, Lior Brimberg, Marc A Schneider and 11 more

Abstract read
In one paragraph

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

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

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

Corrections and comments

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

21 authors.

Samantha HoInstitute of Clinical Neuroimmunology, LMU University Hospital, Ludwig-Maximilians-Universität München, 81377 Munich, Germany; Biomedical Center, Medical Faculty, Ludwig-Maximilians-Universität München, 82152 Planegg-Martinsried, Germany; Graduate School of Systemic Neuroscience, Ludwig-Maximilians-Universität München, 82152 Planegg-Martinsried, Germany.
Hoi Kiu WongInstitute of Clinical Neuroimmunology, LMU University Hospital, Ludwig-Maximilians-Universität München, 81377 Munich, Germany; Biomedical Center, Medical Faculty, Ludwig-Maximilians-Universität München, 82152 Planegg-Martinsried, Germany.
Dorina ShqauInstitute of Clinical Neuroimmunology, LMU University Hospital, Ludwig-Maximilians-Universität München, 81377 Munich, Germany; Biomedical Center, Medical Faculty, Ludwig-Maximilians-Universität München, 82152 Planegg-Martinsried, Germany.
Stephan WinklmeierInstitute of Clinical Neuroimmunology, LMU University Hospital, Ludwig-Maximilians-Universität München, 81377 Munich, Germany; Biomedical Center, Medical Faculty, Ludwig-Maximilians-Universität München, 82152 Planegg-Martinsried, Germany; Department of Translational Immunology, Department of Medicine 3 - Rheumatology and Immunology, Nikolaus-Fiebiger Center for Molecular Medicine, Friedrich-Alexander-Universität (FAU) Erlangen-Nürnberg, Universitätsklinikum Erlangen, 91054 Erlangen, Germany.
Marcus Grobe-EinslerGerman Center for Neurodegenerative Diseases, 53127 Bonn, Germany; Center of Neurology, Department of Parkinson's, Sleep and Movement Disorders, University Hospital Bonn, 53127 Bonn, Germany.
Kevin RostasyChildren's Hospital Datteln, Pediatric Neurology, Witten/Herdecke University, 45711 Datteln, Germany.
Tania KümpfelInstitute of Clinical Neuroimmunology, LMU University Hospital, Ludwig-Maximilians-Universität München, 81377 Munich, Germany.
Franziska S ThalerInstitute of Clinical Neuroimmunology, LMU University Hospital, Ludwig-Maximilians-Universität München, 81377 Munich, Germany; Biomedical Center, Medical Faculty, Ludwig-Maximilians-Universität München, 82152 Planegg-Martinsried, Germany.
Lior BrimbergThe Institute for Molecular Medicine, The Feinstein Institutes for Medical Research, Northwell Health, Manhasset, NY 11030, USA.
Marc A SchneiderTranslational Research Unit, Thoraxklinik at University Hospital Heidelberg, 69126 Heidelberg, Germany; Translational Lung Research Center Heidelberg, German Center for Lung Research (DZL), 69126 Heidelberg, Germany.
Thomas MuleyTranslational Research Unit, Thoraxklinik at University Hospital Heidelberg, 69126 Heidelberg, Germany; Translational Lung Research Center Heidelberg, German Center for Lung Research (DZL), 69126 Heidelberg, Germany.
Atay VuralKoç University Research Center for Translational Medicine (KUTTAM), İstanbul 34450, Türkiye; Koç University Graduate School of Health Sciences, İstanbul 34450, Türkiye; Koç University School of Medicine, Department of Neurology, İstanbul 34450, Türkiye.
Thomas Seifert-HeldDepartment of Neurology, Hospital Murtal, 8720 Knittelfeld, Austria.
Verena EndmayrDepartment of Neurology, Division of Neuropathology and Neurochemistry, Medical University of Vienna, 1090 Vienna, Austria; Comprehensive Center for Clinical Neurosciences and Mental Health, Medical University of Vienna, 1090 Vienna, Austria.
Romana HöftbergerDepartment of Neurology, Division of Neuropathology and Neurochemistry, Medical University of Vienna, 1090 Vienna, Austria; Comprehensive Center for Clinical Neurosciences and Mental Health, Medical University of Vienna, 1090 Vienna, Austria.
Jennifer FaberGerman Center for Neurodegenerative Diseases, 53127 Bonn, Germany; Center of Neurology, Department of Parkinson's, Sleep and Movement Disorders, University Hospital Bonn, 53127 Bonn, Germany; Department of Neuroradiology, University Hospital Bonn, 53127 Bonn, Germany.
Thomas KlopstockFriedrich-Baur-Institute at the Department of Neurology, LMU University Hospital, Ludwig-Maximilians-Universität München, 80336 Munich, Germany; German Center for Neurodegenerative Diseases, 81377 Munich, Germany; Munich Cluster for Systems Neurology (SyNergy), 81377 Munich, Germany.
Silke FrahmTechnology Platform Pluripotent Stem Cells, Max Delbrück Center for Molecular Medicine in the Helmholtz Association, 13125 Berlin, Germany.
Lisa Ann GerdesInstitute of Clinical Neuroimmunology, LMU University Hospital, Ludwig-Maximilians-Universität München, 81377 Munich, Germany; Biomedical Center, Medical Faculty, Ludwig-Maximilians-Universität München, 82152 Planegg-Martinsried, Germany; Munich Cluster for Systems Neurology (SyNergy), 81377 Munich, Germany.
Edgar MeinlInstitute of Clinical Neuroimmunology, LMU University Hospital, Ludwig-Maximilians-Universität München, 81377 Munich, Germany; Biomedical Center, Medical Faculty, Ludwig-Maximilians-Universität München, 82152 Planegg-Martinsried, Germany.
Simone MaderInstitute of Clinical Neuroimmunology, LMU University Hospital, Ludwig-Maximilians-Universität München, 81377 Munich, Germany; Biomedical Center, Medical Faculty, Ludwig-Maximilians-Universität München, 82152 Planegg-Martinsried, Germany; Department of Translational Immunology, Department of Medicine 3 - Rheumatology and Immunology, Nikolaus-Fiebiger Center for Molecular Medicine, Friedrich-Alexander-Universität (FAU) Erlangen-Nürnberg, Universitätsklinikum Erlangen, 91054 Erlangen, Germany; Deutsches Zentrum Immuntherapie, Friedrich-Alexander-Universität (FAU) Erlangen-Nürnberg and Universitätsklinikum Erlangen, 91054 Erlangen, Germany. Electronic address: simone.mader@uk-erlangen.de.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cerebellar ataxias (CAs) encompass a wide spectrum of genetic and sporadic origins, of which a portion is driven by immune-mediated pathomechanisms. While some patients harbor known autoantibodies, assisting diagnosis and treatment, many remain seronegative. Here, we identify synaptophysin (SYP) as an autoantigen in CA by serum IgG staining on primate tissue, combined with human protein array and cell-based assay (CBA). SYP is abundant in presynaptic vesicles and is transiently exposed on the cell surface. Out of 43 patients with CA with synaptic serum reactivity on cerebellar sections, SYP antibodies were identified by CBA in 2 patients. Exposure of human induced pluripotent stem cell (iPSC)-derived glutamatergic neurons to patient's IgG with SYP antibodies causes selective SYP accumulation at the presynaptic membrane. Patient's IgG and SYP monoclonal antibody reduce neuronal populational activity recorded by multi-electrode array. Altogether, we identify SYP as an autoantigen for further stratifying patients with CA. Our functional experiments with SYP antibodies uncover a previously unrecognized mechanism of antibody-mediated synaptic dysfunction.

Indexed as

AutoantibodiesCerebellar AtaxiaSynapsesSynaptophysinAnimalsAutoantigensCerebellumFemaleHumansImmunoglobulin GInduced Pluripotent Stem CellsMaleMiddle AgedNeuronsAutoantibodiesAutoantigensImmunoglobulin GSynaptophysinSYP protein, humanautoantibodiesautoimmunitycerebellar ataxianeuroinflammationsynapsesynaptophysin

Identifiers

PMID42155449
PMCPMC13293949

What Socratic holds

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Registered trials

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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 Socratic graph.