glutamic acid decarboxylase


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Related to glutamic acid decarboxylase: Glutamic Acid Decarboxylase Antibody, GAD65

glutamic acid decarboxylase

Abbreviation: GAD
An enzyme (molecular mass 65 kD) that is found in the brain and the islet cells of the pancreas and participates in the synthesis of gamma-aminobutyric acid. Antibodies to GAD are found in the blood of patients with diabetes mellitus, type, and stiff-person syndrome.
See also: decarboxylase
Medical Dictionary, © 2009 Farlex and Partners
References in periodicals archive ?
Klockgether, "Cerebellar ataxia with glutamic acid decarboxylase autoantibodies," Neurology, vol.
Verlohren et al., "Titre and combination of ICA and autoantibodies to glutamic acid decarboxylase discriminate two clinically distinct types of latent autoimmune diabetes in adults (LADA)," Diabetologia, vol.
Glutamic acid decarboxylase in Parkinson's disease and epilepsy.
In addition, the critical step in GABA biosynthesis is the decarboxylation of glutamate by glutamic acid decarboxylase (GAD).
Harmonization of glutamic acid decarboxylase and islet antigen-2 autoantibody assays for National Institute of Diabetes and Digestive and Kidney Diseases consortia.
Islet cell antibodies and glutamic acid decarboxylase antibodies but not the clinical phenotype help to identify type 1V2 diabetes in patients presenting with type 2 diabetes.
Latent autoimmune diabetes mellitus in adults (LADA): the role of antibodies to glutamic acid decarboxylase in diagnosis and prediction of insulin dependency.
A The company received the two year grant from the United States Department of Veterans Affairs (VA).A Fund will be used by the company for the advancement of NTDDS with Glutamic Acid Decarboxylase (GAD) through preclinical efficacy, toxicology and biodistribution studies, manufacturing and filing of an Investigational New Drug (IND) application with the Food and Drug Administration (FDA).
Latent autoimmune diabetes, which is believed to signal slowly progressive autoimmune [beta]-cell destruction, is a form of type 1 disease characterized by adult on-set; circulating islet cell antibodies and glutamic acid decarboxylase antibodies; and no initial need for insulin therapy.
The appearance of autoantibodies to (3-cell antigens, such as insulin, the 65-kDa isoform of glutamic acid decarboxylase (GAD65)', and protein tyrosine phosphatase-like molecule (IA-2), into the peripheral circulation predicts clinical disease, and the presence of multiple autoantibodies and IA-2 autoantibodies JA2-As) indicates high probability that the disease will appear soon (1, 2).
In 41 infants who had a parent or sibling with type 1 diabetes, significant increases in rotavirus antibodies coincided with the first appearance of insulin autoantibodies in 19 of 23, with antibodies to glutamic acid decarboxylase (GAD) in 14 of 20, and with IA-2 antibodies in 14 of 21 at-risk infants.
The major autoantibodies in DM1 are against islet cells, insulin, a protein tyrosine phosphatase-like protein (IA-2), and the 65-kDa isoform of glutamic acid decarboxylase (GAD65) (1).

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