ArticleFrontiers in immunology2023
Antibody induced seizure susceptibility and impaired cognitive performance in a passive transfer rat model of autoimmune encephalitis.
Article in Frontiers in immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 9 citations in OpenAlex.
- WONOEP XVII appraisal: The immunopathogenesis of epilepsy.Epilepsia · 2026Review
- [18F]fluorodeprenyl-D2 PET can detect and monitor astrogliosis in anti-LGI1-IgG autoimmune encephalitis.European journal of nuclear medicine and molecular imaging · 2026Article
- Research progress on the association between Hashimoto's thyroiditis and autoimmune encephalitis: a review.Frontiers in immunology · 2026Review
- NLRP3 Inflammasome Activation Contributes to Seizure Susceptibility in Anti-NMDAR Encephalitis: Evidence from Patients and a Mouse Model.Molecular neurobiology · 2025Article
- Investigating the Effects of NMDAR and LGI1 Antibodies on Absence Seizures: Insights from Genetic Absence Epilepsy Rats and Acute Pharmacological Model of Absence Seizures.Noro psikiyatri arsivi · 2025Article
- Progress in the preparation of an active immunization model of anti-N-methyl-D-aspartate receptor encephalitis in animals.Frontiers in immunology · 2025Review
- Distinctive sleep complaints and polysomnographic findings in antibody subgroups of autoimmune limbic encephalitis.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2024Article
- The correlation of GluR3B antibody with T lymphocyte subsets and inflammatory factors and their role in the progression of epilepsy.Journal of translational medicine · 2024Article
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective: Autoimmune encephalitis (AE) is a distinct neuro-immunological disorder associated with the production of autoantibodies against neuronal proteins responsible for pharmacoresistant seizures, cognitive decline and behavioral problems. To establish the causal link between leucine-rich glioma inactivated 1 (LGI1) antibody and seizures, we developed an Methods: Total IgG obtained from the pooled sera of NMDAR and LGI1-IgG positive patients with epileptic seizures and healthy subjects was applied chronically every other day for 11 days into the cerebral lateral ventricle. Spontaneous seizure development was followed by electroencephalography. Behavioral tests for memory and locomotor activity were applied before and after the antibody infusions. Then, pentylenetetrazol (PTZ) was administered intraperitoneally to evaluate seizure susceptibility. Immunohistochemistry processed for assessment of hippocampal astrocyte proliferation and expression intensity of target NMDAR and LGI1 antigens. Results: No spontaneous activity was observed during the antibody infusions. PTZ-induced seizure stage was significantly higher in the NMDAR-IgG and LGI1-IgG groups compared to control. Besides, memory deficits were observed in the NMDAR and LGI1-IgG groups. We observed enhanced astrocyte proliferation in NMDAR- and LGI1-IgG groups and reduced hippocampal NMDAR expression in NMDAR-IgG group. Significance: These findings suggest that neuronal surface auto-antibody administration induces seizure susceptibility and disturbed cognitive performance in the passive transfer rat model of LGI1 AE, which could be a potential
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