Type 1 diabetes, also known as insulin-dependent diabetes mellitus (IDDM), results from a chronic autoimmune destruction of the insulin-secreting pancreatic beta cells. Autoimmune destruction of beta cells is thought to be completely asymptomatic until 80-90% of the cells are lost. This process may take years to complete and may occur at any time in all ages. During the preclinical phase, this autoimmune process is marked by circulating autoantibodies to beta cell antigens. These autoantibodies, such as anti-insulin (IAA), anti-glutamic acid decarboxylase (GAD) and anti-tyrosine phosphatase ICA 512 (IA2), are present years before the onset of type 1 diabetes and prior to clinical symptoms. GAD, the enzyme that catalyzes the conversion of glutamate to GABA, has been identified in two isoforms, molecular weight 65.000 (GAD65) and 67.000 (GAD67). Although GAD autoantibodies are found in type 1 diabetes and in the rare neurological disorder Stiff-man syndrome (SMS), the GAD autoantibodies profile in the two diseases differs. Autoantibodies of SMS patients recognize a combination of linear and conformational epitopes of GAD while GAD65 autoantibodies in patients with type 1 diabetes are predominantly directed to the conformational epitopes. GAD65 autoantibodies (GAD65 Abs) are present in 70-80% of newly diagnosed patients with type 1 diabetes. The combination of the autoantibodies to GAD65 and IA2 is highly relevant for risk assessment of type 1 diabetes in children and adolescence. These tests in combination are more sensitive and predictive than ICA in risk groups, e.g. relatives of patients with type 1 diabetes.
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