Medizym® anti-GAD is an enzyme immunoassay (ELISA) for the quantitative determination of autoantibodies to glutamic acid decarboxylase (GAD65 Abs) in human serum. As its name implies, GAD is responsible for the catalysis for glutamate to gamma-Aminobutyric acid (GABA), an essential neurotransmitter in the mammalian system. Antibodies against the GAD65 isoform have been detected in a variety of neurological autoimmune disorders. Additionally, the GAD65 autoantibody is the major antibody for the pancreatic islets and a serological marker for the predisposition of type 1 diabetes and other autoimmune disorders that accompany it.
- Microtiter plate. 12 breakable strips with 8 wells each (96 wells total) coated with human recombinant GAD65. The plate is supplied in a vacuum sealed bag with desicant.
- Concentrated Wash Buffer. 125 mL of 10x concentrated wash buffer
- Streptavidin-peroxidase (SA-POD).7 mL of 20x concentrated enzyme conjugate
- 15 mL of ready to use TMB
- Stop Solution. 12 mL of 0.25 M sulfuric acid. Ready to use
- Diluent for SA-POD. 15 mL of ready to use dilution buffer
- GAD65-Biotin. 3 vials of lyophilized biotin conjugated GAD65
- Diluent for GAD65-Biotin. 2 vials of 15 mL dilution buffer. Ready to use
- Negative Control.7 mL of ready to use negative control
- Positive Control. 7 mL of ready to use positive control with a lot-dependent concentration of GAD65
- 5 vials, 0.7 mL each of ready to use calibrator material.
Type 1 diabetes, also known as insulin-dependent diabetes mellitus (IDDM), results from a chronic autoimmune destruction of the insulin-secreting pancreatic beta cells, probably initiated by exposure of genetically susceptible host to environmental agents. 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 discovered type 1 diabetes.
The combination of the autoantibodies to GAD65 and IA2 is highly relevant 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.
GAD65 Abs also occurs in a subset of adults with type 2 diabetes. These subjects can have pronounced hyperglycemia, and after therapy with oral hypoglycemic agents for several months to years they may become insulin dependent. Therefore, these patients are thought to have a slowly progressive form of type 1 diabetes, often called latent diabetes or latent autoimmune diabetes in adults (LADA).