ArticleFrontiers in immunology2017
Selective Limbic Blood-Brain Barrier Breakdown in a Feline Model of Limbic Encephalitis with LGI1 Antibodies.
Article in Frontiers in immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 60 citations in OpenAlex.
- Effectiveness and safety of efgartigimod in patients with anti-NMDAR or anti-LGI1 encephalitis and itsNeuroprotection (Chichester, England) · 2026Article
- Diencephalic integrity explains aspects of hippocampal amnesia.Cerebral cortex (New York, N.Y. : 1991) · 2026Article
- Immunopathological mechanisms in autoimmune encephalitis: from pathogenesis to targeted therapies.Frontiers in immunology · 2026Review
- Restoring brain barriers: an innovative approach for treating neurological disorders.Fluids and barriers of the CNS · 2025Review
- The Clinical Trial Landscape in Autoimmune Encephalitis: Challenges and Opportunities.Neurology · 2025Review
- The Involvement of Glial Cells in Blood-Brain Barrier Damage in Neuroimmune Diseases.International journal of molecular sciences · 2024Review
- Origin and significance of leucine-rich glioma-inactivated 1 antibodies in cerebrospinal fluid.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2024Article
- LGI1 encephalitis: potentially complement-activating anti-LGI1-IgG subclasses 1/2/3 are associated with the development of hippocampal sclerosis.Journal of neurology · 2024Article
- CSF Findings in Chinese Patients with NMDAR, LGI1 and GABABR Antibody-Associated Encephalitis.Journal of inflammation research · 2024Article
- Review
- Abnormal DNA methylation analysis of leucine-rich glioma-inactivated 1 antibody encephalitis reveals novel methylation-driven genes related to prognostic and clinical features.Clinical epigenetics · 2023Article
- Parallel roles of neuroinflammation in feline and human epilepsies.Veterinary journal (London, England : 1997) · 2022Review
- CSF Findings in Acute NMDAR and LGI1 Antibody-Associated Autoimmune Encephalitis.Neurology(R) neuroimmunology & neuroinflammation · 2021Article
- Perisylvian vulnerability to postencephalitic epilepsy.Clinical neurophysiology : official journal of the International Federation of Clinical Neurophysiology · 2020Article
- Companion animal models of neurological disease.Journal of neuroscience methods · 2020Review
- Hippocampal network abnormalities explain amnesia after VGKCC-Ab related autoimmune limbic encephalitis.Journal of neurology, neurosurgery, and psychiatry · 2019Article
- Article
- Review
- Novel Object Recognition in Rats With NMDAR Dysfunction in CA1 After Stereotactic Injection of Anti-NMDAR Encephalitis Cerebrospinal Fluid.Frontiers in neurology · 2019Article
- [Principles of autoimmune and paraneoplastic encephalitis].Der Nervenarzt · 2018Review
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
Human leucine-rich glioma-inactivated protein 1 encephalitis (LGI1) is an autoimmune limbic encephalitis in which serum and cerebrospinal fluid contain antibodies targeting LGI1, a protein of the voltage gated potassium channel (VGKC) complex. Recently, we showed that a feline model of limbic encephalitis with LGI1 antibodies, called feline complex partial seizures with orofacial involvement (FEPSO), is highly comparable to human LGI1 encephalitis. In human LGI1 encephalitis, neuropathological investigations are difficult because very little material is available. Taking advantage of this natural animal model to study pathological mechanisms will, therefore, contribute to a better understanding of its human counterpart. Here, we present a brain-wide histopathological analysis of FEPSO. We discovered that blood-brain barrier (BBB) leakage was present not only in all regions of the hippocampus but also in other limbic structures such as the subiculum, amygdale, and piriform lobe. However, in other regions, such as the cerebellum, no leakage was observed. In addition, this brain-region-specific immunoglobulin leakage was associated with the breakdown of endothelial tight junctions. Brain areas affected by BBB dysfunction also revealed immunoglobulin and complement deposition as well as neuronal cell death. These neuropathological findings were supported by magnetic resonance imaging showing signal and volume increase in the amygdala and the piriform lobe. Importantly, we could show that BBB disturbance in LGI1 encephalitis does not depend on T cell infiltrates, which were present brain-wide. This finding points toward another, so far unknown, mechanism of opening the BBB. The limbic predilection sites of immunoglobulin antibody leakage into the brain may explain why most patients with LGI1 antibodies have a limbic phenotype even though LGI1, the target protein, is ubiquitously distributed across the central nervous system.
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