ArticleThe Journal of clinical investigation2022
Schwann cell nodal membrane disruption triggers bystander axonal degeneration in a Guillain-Barré syndrome mouse model.
Article in The Journal of clinical investigation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 33 citations in OpenAlex.
- α2-3-sialylated glycosphingolipids in neuroinflammation, immunity, and programmed cell death: mechanistic evidence and context-dependent regulation: a comprehensive review.Frontiers in immunology · 2026Review
- A rare presentation of CASPR2-associated Morvan syndrome overlapping with GM1-positive AMSAN: a case report.Frontiers in immunology · 2026Article
- The Neuromuscular Junction: A Shared Vulnerability in Aging and Disease.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Review
- The changing landscape of primary autoimmune neuropathies.Nature reviews. Neurology · 2025Review
- Pathologic and Therapeutic Schwann Cells.Cells · 2025Review
- Basic Pathological Mechanisms in Peripheral Nerve Diseases.International journal of molecular sciences · 2025Review
- Guillain-Barré syndrome.Nature reviews. Disease primers · 2024Article
- Review
- Guillain-Barré syndrome: a comprehensive review.European journal of neurology · 2024Review
- P2X7 receptor antagonists modulate experimental autoimmune neuritis via regulation of NLRP3 inflammasome activation and Th17 and Th1 cell differentiation.Journal of neuroinflammation · 2024Article
- Immune-Mediated Neuropathies: Pathophysiology and Management.International journal of molecular sciences · 2023Review
- The endogenous calpain inhibitor calpastatin attenuates axon degeneration in murine Guillain-Barré syndrome.Journal of the peripheral nervous system : JPNS · 2023Article
- Axolemmal nanoruptures arising from paranodal membrane injury induce secondary axon degeneration in murine Guillain-Barré syndrome.Journal of the peripheral nervous system : JPNS · 2023Article
- Neuron-Schwann cell interactions in peripheral nervous system homeostasis, disease, and preclinical treatment.Frontiers in cellular neuroscience · 2023Review
- Neuromuscular disease: 2023 update.Free neuropathology · 2023Article
- Review
- Real time imaging of intra-axonal calcium flux in an explant mouse model of axonal Guillain-Barré syndrome.Experimental neurology · 2022Article
- Glial cells and neurologic autoimmune disorders.Frontiers in cellular neuroscience · 2022Review
- Complement inhibition prevents glial nodal membrane injury in a GM1 antibody-mediated mouse model.Brain communications · 2022Article
- Case report: Recreational nitrous oxide abuse triggered peripheral neuropathy possibly through the immune-mediated pathogenesis.Frontiers in neurology · 2022Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
In Guillain-Barré syndrome (GBS), both axonal and demyelinating variants can be mediated by complement-fixing anti-GM1 ganglioside autoantibodies that target peripheral nerve axonal and Schwann cell (SC) membranes, respectively. Critically, the extent of axonal degeneration in both variants dictates long-term outcome. The differing pathomechanisms underlying direct axonal injury and the secondary bystander axonal degeneration following SC injury are unresolved. To investigate this, we generated glycosyltransferase-disrupted transgenic mice that express GM1 ganglioside either exclusively in neurons [GalNAcT-/--Tg(neuronal)] or glia [GalNAcT-/--Tg(glial)], thereby allowing anti-GM1 antibodies to solely target GM1 in either axonal or SC membranes, respectively. Myelinated-axon integrity in distal motor nerves was studied in transgenic mice exposed to anti-GM1 antibody and complement in ex vivo and in vivo injury paradigms. Axonal targeting induced catastrophic acute axonal disruption, as expected. When mice with GM1 in SC membranes were targeted, acute disruption of perisynaptic glia and SC membranes at nodes of Ranvier (NoRs) occurred. Following glial injury, axonal disruption at NoRs also developed subacutely, progressing to secondary axonal degeneration. These models differentiate the distinctly different axonopathic pathways under axonal and glial membrane targeting conditions, and provide insights into primary and secondary axonal injury, currently a major unsolved area in GBS research.
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Registered trials
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.