GLUTAMIC ACID DECARBOXYLASE AB
- GLUTAMIC ACID DECARBOXYLASE AB
- Start Date
- Expiration Date
- GAD, GAD Antibody, GAD65 Antibody
- CPT Codes
- Reference Test
- Transport Info
Centrifuge and immediately transfer serum to separate plastic tube
- Fasting Required?
- Patient Instructions
- Reference Range
Less than 5 U/mL
Enzyme-Linked Immunosorbent Assay (ELISA)
Glutamic acid decarboxylase (GAD) is the enzyme responsible for the synthesis of neurotransmitter gamma-aminobutyric acid in neurons and pancreatic beta cells. It is represented by two isoforms, GAD65 and GAD67, which are the products of two different genes. GAD65 is the dominant autoantigen in stiff-person syndrome (SPS) and insulin-dependent diabetes mellitus (IDDM).
In SPS, the immune system makes antibodies against GAD65. GAD65 plays an important role in the production of gamma-aminobutyric acid (GABA), a neurotransmitter that inhibits certain activity in the spinal cord and brain.
Type I diabetes, IDDM, accounts for approximately 15% of the diabetic population. IDDM is generally seen in children and young adults, but it can strike at any age. Insulin deficiency results in autoimmune destruction of insulin producing pancreatic beta cells. Clinical onset of diabetes does not occur until 80-90% of these cells are destroyed. Prior to clinical onset, type1 diabetes can be characterized by lymphocytic infiltration of the islet cells and various circulating autoantibodies. Measuring these autoantibodies as disease markers at the pre-diabetic stage affords an opportunity to predict and prevent the clinical onset of the disease.
GAD65 antibodies have been found in 70-90% of pre-diabetic and Type 1 diabetic patients. It is the most sensitive single marker for identifying individuals at risk of developing diabetes. GAD65 is more prevalent in older children and late-onset Type 1 diabetes and the marker has been shown to be detected ten years prior to disease onset.