ReviewJournal of immunology research2017
Pathogenic Roles of Glutamic Acid Decarboxylase 65 Autoantibodies in Cerebellar Ataxias.
Review in Journal of immunology research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 61 citations in OpenAlex.
- Unidirectional Palsy of Torsional Saccades in Ataxia Associated with Anti-GAD Antibody.Cerebellum (London, England) · 2026Article
- Clinical Features of Glutamic Acid Decarboxylase-65 Neurological Autoimmunity: A Case Series From China.CNS neuroscience & therapeutics · 2025Article
- A candidate projective neuron type of the cerebellar cortex: the synarmotic neuron.European journal of histochemistry : EJH · 2024Review
- Consensus Paper: Latent Autoimmune Cerebellar Ataxia (LACA).Cerebellum (London, England) · 2024Article
- Review
- Cold Plasma Treatment Increases Bioactive Metabolites in Oat (Avena sativa L.) Sprouts and Enhances In Vitro Osteogenic Activity of their Extracts.Plant foods for human nutrition (Dordrecht, Netherlands) · 2023Article
- A Case of Anti-GAD 65 Autoimmune Encephalitis Associated with Focal Segmental Stiff-Person Syndrome.Brain sciences · 2023Article
- Advances in the Pathogenesis of Auto-antibody-Induced Cerebellar Synaptopathies.Cerebellum (London, England) · 2023Review
- Case Report: Extraocular muscles paralysis associated with GAD65 antibody: a case series study.Frontiers in immunology · 2023Article
- Autoantibodies directed against glutamate decarboxylase interfere with glucose-stimulated insulin secretion in dispersed rat islets.International journal of experimental pathology · 2022Article
- Article
- Acute Cerebellar Inflammation and Related Ataxia: Mechanisms and Pathophysiology.Brain sciences · 2022Review
- A Breakdown of Immune Tolerance in the Cerebellum.Brain sciences · 2022Review
- The Role of Alpha-Synuclein Autoantibodies in the Induction of Brain Inflammation and Neurodegeneration in Aged Humans.Frontiers in aging neuroscience · 2022Article
- The clinical relevance of anti-glutamic acid decarboxylase antibodies in children with encephalitis/encephalopathy.Frontiers in neuroscience · 2022Article
- Mechanisms of Ethanol-Induced Cerebellar Ataxia: Underpinnings of Neuronal Death in the Cerebellum.International journal of environmental research and public health · 2021Review
- Cerebellar long-term depression and auto-immune target of auto-antibodies: the concept of LTDpathies.Molecular biomedicine · 2021Review
- Immune-Mediated Cerebellar Ataxias: Clinical Diagnosis and Treatment Based on Immunological and Physiological Mechanisms.Journal of movement disorders · 2021Article
- Fundamental Mechanisms of Autoantibody-Induced Impairments on Ion Channels and Synapses in Immune-Mediated Cerebellar Ataxias.International journal of molecular sciences · 2020Review
- GAD antibodies in neurological disorders - insights and challenges.Nature reviews. Neurology · 2020Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
Reports suggesting a pathogenic role of autoantibodies directed against glutamic acid decarboxylase 65 (GAD65Abs) in cerebellar ataxias (CAs) are reviewed, and debatable issues such as internalization of antibodies by neurons and roles of epitopes are discussed. GAD65 is one of two enzymes that catalyze the conversion of glutamate to the inhibitory neurotransmitter gamma-aminobutyric acid (GABA). A pathogenic role of GAD65Ab in CAs is suggested by in vivo and in vitro studies. (1) Intracerebellar administration of cerebrospinal fluid (CSF) immunoglobulins (IgGs) obtained from GAD65Ab-positive CA patients impairs cerebellar modulation of motor control in rats. (2) CSF IgGs act on terminals of GABAergic neurons and decrease the release of GABA in cerebellar slices from rats and mice. (3) Absorption of GAD65Ab by recombinant GAD65 diminishes the above effects, and monoclonal human GAD65Ab (b78) mimic the effects of CSF IgGs in vivo and in vitro. Studies using GAD65-KO mice confirm that the target molecule is GAD65. (4) Notably, the effects of GAD65Ab depend on the epitope specificity of the monoclonal GAD65Ab. Taken together, these results indicate that epitope-specific GAD65Ab-induced impairment of GABA release is involved in the pathogenesis of GAD65Ab-positive CA and support the early detection of GAD65Ab-associated CA to initiate immunotherapy before irreversible neuronal death in the cerebellum.
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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.