1 Autoimmune DM is characterised by the presence of one or more islet-specific autoantibodies, including islet cell autoantibodies (ICA), insulin (IAA) and autoantibodies directed against the three major islet autoantigens - glutamic acid decarboxylase
65 (GADA), protein tyrosine phosphatase IA-2A and its isoform IA-2b/phogrin (IA-2bA).
Spectrum of neurological syndromes associated with glutamic acid decarboxylase
antibodies: diagnostic clues for this association.
Epilepsy in mice deficient in the 65-kDa isoform of glutamic acid decarboxylase
32%) and gadA/B and glutamic acid decarboxylase
Increased anxiety and altered responses to anxiolytics in mice deficient in the 65-kDa isoform of glutamic acid decarboxylase
Glutamic acid decarboxylase
antibodies (GADA) is the most important factor for prediction of insulin therapy within 3 years in young adult diabetic patients not classified as Type 1 diabetes on clinical grounds.
Patients with T1D commonly produce autoantibodies to islet cell cytoplasm (ICA), native insulin (insulin autoantibodies, or IAAs), the 65-kDa isoform of glutamic acid decarboxylase
(GAD65), the insulinoma antigen 2 protein (LA-2), and variants of zinc transporter 8 (ZnT8).
Autoantibody Autoantigen ICA The ICA autoantigens are not well defined but include a sialoglycoconjugate and glutamic acid decarboxylase
(34) 1AA Insulin (proinsulin antibodies have also been demonstrated) GADA Glutamic acid decarboxylase
(GAD65 > GAD67) 1A-2A A protein tyrosine phosphatase (PTP) ZnT8A Zinc transporter-8 that transports zinc into insulin secretory granules ICA = lslet cell cytoplasmic autoantibodies; IAA = Insulin autoantibodies; GADA = Glutamic acid decarboxylase
autoantibodies; 1A-2A = Insulinoma associated-2 autoantibodies; ZnT8A = Zinc trasnporter-8 autoantibodies Table 1.
One of those studies, in which new-onset type 1 patients were treated with the antigen glutamic acid decarboxylase
(GAD), produced negative results.
Diabetes mellitus decreases the expression of calcitonin-gene related peptide, gamma-amino butyric acid and glutamic acid decarboxylase
in human pancreatic islet cells.
Diamyd is a glutamic acid decarboxylase
(GAD)-based therapy for the treatment and prevention of type 1 diabetes and associated conditions.
However, it had no effect on the abundance of the expression of glutamic acid decarboxylase
(GAD), suggesting that obovatol might not activate GAD.