ArticleJournal of neural transmission (Vienna, Austria : 1996)2015
Stiff person-syndrome IgG affects presynaptic GABAergic release mechanisms.
Article in Journal of neural transmission (Vienna, Austria : 1996), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed, 15 citations in OpenAlex.
- Forkhead box versus NF-κB hippocampal snRNA-seq profiles distinguish anti-Drebrin- and anti-GAD65-positive encephalitis.Journal of neuroinflammation · 2026Article
- Chimeric antigen receptor T-cell therapy for stiff-person syndrome: bridging innovation and clinical challenges in neuroimmunology.Therapeutic advances in neurological disorders · 2025Review
- Stiff-person syndrome and related disorders - diagnosis, mechanisms and therapies.Nature reviews. Neurology · 2024Review
- Increased T- and B-cells associated with the phenotype of autoimmune limbic encephalitis with mainly memory dysfunction.Journal of translational autoimmunity · 2022Article
- Article
- Anti-GAD65 Containing Cerebrospinal Fluid Does not Alter GABAergic Transmission.Frontiers in cellular neuroscience · 2016Article
- Serum from a Patient with GAD65 Antibody-Associated Limbic Encephalitis Did Not Alter GABAergic Neurotransmission in Cultured Hippocampal Networks.Frontiers in neurology · 2015Article
- Interactions of Human Autoantibodies with Hippocampal GABAergic Synaptic Transmission - Analyzing Antibody-Induced Effects ex vivo.Frontiers in neurology · 2015Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The majority of patients with stiff person-syndrome (SPS) are characterized by autoantibodies to glutamate decarboxylase 65 (GAD65). In previous passive-transfer studies, SPS immunoglobulin G (IgG) induced SPS core symptoms. We here provide evidence that SPS-IgG causes a higher frequency of spontaneous vesicle fusions. Sustained GABAergic transmission and presynaptic GABAergic vesicle pool size remained unchanged. Since these findings cannot be attributed to anti-GAD65 autoantibodies alone, we propose that additional autoantibodies with so far undefined antigen specificity might affect presynaptic release mechanisms.
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Registered trials
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