ArticleJournal of neuroinflammation2013
Two new cases of anti-Ca (anti-ARHGAP26/GRAF) autoantibody-associated cerebellar ataxia.
Article in Journal of neuroinflammation, 2013. 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, 45 citations in OpenAlex.
- Non-paraneoplastic Autoimmune Cerebellar Ataxia with Sensory Ataxia Associated with the Anti-Ca/ARHGAP26 Antibody: A Case Report.Cerebellum (London, England) · 2026Article
- Untreated anti-Ca/ARHGAP26 autoantibody-associated cerebellar ataxia progressing over 27 years.Journal of neurology · 2023Article
- Rho GTPase-activating protein 17 (ARHGAP17) as additional autoimmune target in ARHGAP26-IgG/anti-Ca autoantibody-associated autoimmune encephalitis.Journal of neurology · 2023Article
- Septin-5 and -7-IgGs: Neurologic, Serologic, and Pathophysiologic Characteristics.Annals of neurology · 2022Article
- Rho GTPase-activating protein 10 (ARHGAP10/GRAF2) is a novel autoantibody target in patients with autoimmune encephalitis.Journal of neurology · 2022Article
- Novelties in Autoimmune and Paraneoplastic Cerebellar Ataxias: Twenty Years of Progresses.Cerebellum (London, England) · 2022Review
- Inositol 1,4,5-trisphosphate receptor type 1 autoantibody (ITPR1-IgG/anti-Sj)-associated autoimmune cerebellar ataxia, encephalitis and peripheral neuropathy: review of the literature.Journal of neuroinflammation · 2022Review
- The role of GTPase-activating protein ARHGAP26 in human cancers.Molecular and cellular biochemistry · 2022Review
- GTPase Regulator Associated with Focal Adhesion Kinase 1 (GRAF1) Immunoglobulin-Associated Ataxia and Neuropathy.Movement disorders clinical practice · 2020Article
- Immunological Bases of Paraneoplastic Cerebellar Degeneration and Therapeutic Implications.Frontiers in immunology · 2020Review
- Anti-ARHGAP26 Autoantibodies Are Associated With Isolated Cognitive Impairment.Frontiers in neurology · 2018Article
- Antibodies to inositol 1,4,5-triphosphate receptor 1 in patients with cerebellar disease.Neurology(R) neuroimmunology & neuroinflammation · 2017Article
- Inositol 1,4,5-trisphosphate receptor type 1 autoantibodies in paraneoplastic and non-paraneoplastic peripheral neuropathy.Journal of neuroinflammation · 2016Article
- Consensus Paper: Neuroimmune Mechanisms of Cerebellar Ataxias.Cerebellum (London, England) · 2016Review
- 'Medusa head ataxia': the expanding spectrum of Purkinje cell antibodies in autoimmune cerebellar ataxia. Part 2: Anti-PKC-gamma, anti-GluR-delta2, anti-Ca/ARHGAP26 and anti-VGCC.Journal of neuroinflammation · 2015Review
- 'Medusa-head ataxia': the expanding spectrum of Purkinje cell antibodies in autoimmune cerebellar ataxia. Part 1: Anti-mGluR1, anti-Homer-3, anti-Sj/ITPR1 and anti-CARP VIII.Journal of neuroinflammation · 2015Review
- Antibodies to the inositol 1,4,5-trisphosphate receptor type 1 (ITPR1) in cerebellar ataxia.Journal of neuroinflammation · 2014Article
- GRAF1a is a brain-specific protein that promotes lipid droplet clustering and growth, and is enriched at lipid droplet junctions.Journal of cell science · 2014Article
- Carbonic anhydrase-related protein VIII antibodies and paraneoplastic cerebellar degeneration.Neuropathology and applied neurobiology · 2014Article
- Paraneoplastic neurological syndromes.Clinical and experimental immunology · 2014Review
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recently, we discovered a novel serum and cerebrospinal fluid (CSF) autoantibody (anti-Ca) to Purkinje cells in a patient with autoimmune cerebellar ataxia (ACA) and identified the RhoGTPase-activating protein 26 (ARHGAP26; alternative designations include GTPase regulator associated with focal adhesion kinase pp125, GRAF, and oligophrenin-1-like protein, OPHN1L) as the target antigen. Here, we report on two new cases of ARHGAP26 autoantibody-positive ACA that were first diagnosed after publication of the index case study. While the index patient developed ACA following an episode of respiratory infection with still no evidence for malignancy 52 months after onset, neurological symptoms heralded ovarian cancer in one of the patients described here. Our finding of anti-Ca/anti-ARHGAP26 antibodies in two additional patients supports a role of autoimmunity against ARHGAP26 in the pathogenesis of ACA. Moreover, the finding of ovarian cancer in one of our patients suggests that anti-Ca/anti-ARHGAP26-positive ACA might be of paraneoplastic aetiology in some cases. In conclusion, testing for anti-Ca/anti-ARHGAP26 should be included in the diagnostic work-up of patients with ACA, and an underlying tumour should be considered in patients presenting with anti-Ca/ARHGAP26 antibody-positive ACA.
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Registered trials
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