Glutamic Acid Decarboxylase Antibody

Chiara Crotti, Carlo Selmi

Research output: Chapter in Book/Report/Conference proceedingChapter


Glutamic acid decarboxylase (GAD) catalyzes the conversion of glutamic acid into gamma-amino butyric acid within pancreatic islet β cells. Autoantibodies against GAD (GADA) are found in patients with type 1 diabetes mellitus (T1DM), stiff-person syndrome, and epilepsy. Both GAD forms are recognized by GADA, but GAD65 is the predominant autoantigen being recognized in 65% of patients. Up to 90% of children and adolescents who will develop T1DM and patients with latent autoimmune diabetes in adults (LADA) recognize either form. Unlike other islet autoantibodies, GADA persist for many years after the diagnosis in a significant proportion of patients with T1DM and can thus characterize long-standing diabetes. Indeed, it has been demonstrated that the presence of multiple autoantibodies is associated with a high risk of developing diabetes. The identification of GAD as a major autoantigen in T1DM is the basis for new therapy approaches to inhibit the progression of disease by inducing tolerance in GAD-reactive T cells.

Original languageEnglish
Title of host publicationAutoantibodies: Third Edition
PublisherElsevier B.V.
Number of pages5
ISBN (Print)9780444563781
Publication statusPublished - Dec 2013


  • GAD65
  • GAD67
  • Gamma-amino butyric acid
  • Insulin
  • Islet cell autoimmunity
  • Isoforms
  • Pancreatic islets
  • Type 1 diabetes mellitus

ASJC Scopus subject areas

  • Immunology and Microbiology(all)


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