ArticleNeuron2018
Immune or Genetic-Mediated Disruption of CASPR2 Causes Pain Hypersensitivity Due to Enhanced Primary Afferent Excitability.
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Article in Neuron, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 98 papers, 2 of them syntheses that pooled it.
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98citing papers in PubMed, 2 pooled it
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Who cites it
98 citing papers in PubMed, 2 syntheses or guidelines pooled it, 182 citations in OpenAlex.
- Convergent blood-brain barrier breakdown in schizophrenia and autism spectrum disorders: a systematic review of preclinical animal models.Fluids and barriers of the CNS · 2026Pooled it
- Systematic review of the clinical spectrum of CASPR2 antibody syndrome.Journal of neurology · 2020Pooled it
- Beyond Nerve Hyperexcitability: Potential Implications of Cerebrospinal Fluid CASPR2 Antibodies for Central Pain Processing in Isaacs Syndrome: A Case-Based Systematic Review.Pain and therapy · 2026Article
- The cascade to pathogenicity in autoantibody-mediated CNS diseases.Brain : a journal of neurology · 2026Review
- Recent advances in autoantibody-mediated pain.Current opinion in supportive and palliative care · 2026Review
- ATP13A4 gates extracellular polyamine levels to control excitatory synaptogenesis.Nature communications · 2026Article
- Isaacs syndrome associated with polyarteritis nodosa.BMJ case reports · 2026Article
- Pathogenic IgG from long COVID patients with neurological sequelae triggers sensitive but not cognitive impairments upon transfer into mice.Acta neuropathologica · 2026Article
- Transfer of IgG from long COVID patients induces symptomology in mice.Cell reports. Medicine · 2026Article
- Autoantibodies as drivers of neuropathic pain.Trends in molecular medicine · 2026Review
- CASPR2 Autoimmune Antibodies Induce Neuronal Hyperactivity in Human Brain Organoids.Journal of neurochemistry · 2026Article
- Article
- The neuroimmune microenvironment of peripheral nerve injury: mechanisms, pathophysiology, and therapeutic implications.Frontiers in surgery · 2026Review
- Article
- Aβ low threshold mechanoreceptors contribute to sensory abnormalities in fibromyalgia.Brain : a journal of neurology · 2025Article
- Fc gamma receptor IIa signaling from spinal cord astrocytes promotes neuropathic pain in rats.The journal of pain · 2025Article
- Altered Primary Somatosensory Neuron Development in a Pten Heterozygous Model for Autism Spectrum Disorder.Autism research : official journal of the International Society for Autism Research · 2025Article
- Neuromyotonia and CASPR2 Antibodies: Electrophysiological Clues to Disease Pathophysiology.Biomolecules · 2025Review
- Histone lactylation regulates DOCK4 to control heat nociception and supports Dynein-mediated Nav1.7 trafficking.Nature communications · 2025Article
- Prevalence of the anti-CASPR2 autoantibody in patients with somatic symptom disorder accompanied by medically unexplained pain.Brain, behavior, & immunity - health · 2025Article
38 more citing papers are in PubMed but not listed here.
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Authors and funding
40 authors at 8 institutions in 4 countries.
John M DawesNuffield Department of Clinical Neurosciences, University of Oxford, Oxford OX3 9DU, UK.
Greg A WeirNuffield Department of Clinical Neurosciences, University of Oxford, Oxford OX3 9DU, UK.
Steven J MiddletonNuffield Department of Clinical Neurosciences, University of Oxford, Oxford OX3 9DU, UK.
Ryan PatelDepartment of Neuroscience, Physiology and Pharmacology, University College London, London WC1E 6BT, UK.
Kim I ChisholmNeurorestoration Group, Wolfson Centre for Age-Related Diseases, King's College London, London SE1 1UL, UK.
Philippa PettingillNuffield Department of Clinical Neurosciences, University of Oxford, Oxford OX3 9DU, UK.
Liam J PeckNuffield Department of Clinical Neurosciences, University of Oxford, Oxford OX3 9DU, UK.
Joseph SheridanNuffield Department of Clinical Neurosciences, University of Oxford, Oxford OX3 9DU, UK.
Akila ShakirNuffield Department of Clinical Neurosciences, University of Oxford, Oxford OX3 9DU, UK.
Leslie JacobsonNuffield Department of Clinical Neurosciences, University of Oxford, Oxford OX3 9DU, UK.
Maria Gutierrez-MecinasInstitute of Neuroscience and Psychology, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow G12 8QQ, UK.
Jorge GalinoNuffield Department of Clinical Neurosciences, University of Oxford, Oxford OX3 9DU, UK.
Jan WalcherMolecular Physiology of Somatic Sensation, Max Delbrück Center for Molecular Medicine, Berlin, Germany.
Johannes KühnemundMolecular Physiology of Somatic Sensation, Max Delbrück Center for Molecular Medicine, Berlin, Germany.
Hannah KuehnNuffield Department of Clinical Neurosciences, University of Oxford, Oxford OX3 9DU, UK.
Maria D SannaNuffield Department of Clinical Neurosciences, University of Oxford, Oxford OX3 9DU, UK.
Bethan LangNuffield Department of Clinical Neurosciences, University of Oxford, Oxford OX3 9DU, UK.
Alex J ClarkNuffield Department of Clinical Neurosciences, University of Oxford, Oxford OX3 9DU, UK.
Andreas C ThemistocleousNuffield Department of Clinical Neurosciences, University of Oxford, Oxford OX3 9DU, UK.
Noboru IwagakiInstitute of Neuroscience and Psychology, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow G12 8QQ, UK.
Steven J WestNuffield Department of Clinical Neurosciences, University of Oxford, Oxford OX3 9DU, UK.
Karolina WerynskaNuffield Department of Clinical Neurosciences, University of Oxford, Oxford OX3 9DU, UK.
Liam CarrollNuffield Department of Clinical Neurosciences, University of Oxford, Oxford OX3 9DU, UK.
Teodora TrendafilovaNuffield Department of Clinical Neurosciences, University of Oxford, Oxford OX3 9DU, UK.
David A MenassaNuffield Department of Clinical Neurosciences, University of Oxford, Oxford OX3 9DU, UK.
Maria Pia GiannoccaroNuffield Department of Clinical Neurosciences, University of Oxford, Oxford OX3 9DU, UK.
Ester CoutinhoNuffield Department of Clinical Neurosciences, University of Oxford, Oxford OX3 9DU, UK.
Ilaria CervelliniNuffield Department of Clinical Neurosciences, University of Oxford, Oxford OX3 9DU, UK.
Damini TewariNeurorestoration Group, Wolfson Centre for Age-Related Diseases, King's College London, London SE1 1UL, UK.
Camilla BuckleyNuffield Department of Clinical Neurosciences, University of Oxford, Oxford OX3 9DU, UK.
M Isabel LeiteNuffield Department of Clinical Neurosciences, University of Oxford, Oxford OX3 9DU, UK.
Hendrik WildnerInstitute of Pharmacology and Toxicology, University of Zurich, Winterthurerstrasse 190, 8057 Zürich, Switzerland.
Hanns Ulrich ZeilhoferInstitute of Pharmacology and Toxicology, University of Zurich, Winterthurerstrasse 190, 8057 Zürich, Switzerland; Institute of Pharmaceutical Sciences, Swiss Federal Institute of Technology (ETH) Zurich, Vladimir-Prelog-Weg 10, 8093 Zurich, Switzerland.
Elior PelesDepartment of Molecular Cell Biology, Weizmann Institute of Science, Rehovot 76100, Israel.
Andrew J ToddInstitute of Neuroscience and Psychology, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow G12 8QQ, UK.
Stephen B McMahonNeurorestoration Group, Wolfson Centre for Age-Related Diseases, King's College London, London SE1 1UL, UK.
Anthony H DickensonDepartment of Neuroscience, Physiology and Pharmacology, University College London, London WC1E 6BT, UK.
Gary R LewinMolecular Physiology of Somatic Sensation, Max Delbrück Center for Molecular Medicine, Berlin, Germany.
Angela VincentNuffield Department of Clinical Neurosciences, University of Oxford, Oxford OX3 9DU, UK.
David L BennettNuffield Department of Clinical Neurosciences, University of Oxford, Oxford OX3 9DU, UK. Electronic address: david.bennett@ndcn.ox.ac.uk.
University of Oxford · GBKing's College London · GBMax Delbrück Center · DEUniversity of Glasgow · GBUniversity College London · GBETH Zurich · CHUniversity of Zurich · CHWeizmann Institute of Science · IL
Funding
Medical Research Council G0401222Medical Research Council G0501898Medical Research Council MR/M02394X/1Wellcome Trust 202747/Z/16/Z
Abstract
Human autoantibodies to contactin-associated protein-like 2 (CASPR2) are often associated with neuropathic pain, and CASPR2 mutations have been linked to autism spectrum disorders, in which sensory dysfunction is increasingly recognized. Human CASPR2 autoantibodies, when injected into mice, were peripherally restricted and resulted in mechanical pain-related hypersensitivity in the absence of neural injury. We therefore investigated the mechanism by which CASPR2 modulates nociceptive function. Mice lacking CASPR2 (Cntnap2
Indexed as
AnimalsCells, CulturedFemaleGanglia, SpinalHumansImmunization, PassiveImmunoglobulin GMaleMechanotransduction, CellularMembrane ProteinsMice, Inbred C57BLMice, KnockoutNerve Tissue ProteinsNociceptive PainPosterior Horn CellsSensory Receptor CellsCNTNAP2 protein, mouseImmunoglobulin GMembrane ProteinsNerve Tissue ProteinsShaker Superfamily of Potassium ChannelsautismautoantibodyCASPR2CNTNAP2DRGKv1mechanosensationpainsensory neuronvoltage-gated potassium channel
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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 OpenQuestion graph.