GAD2抗体

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     Black line: Control Antigen (100 ng); Purple line: Antigen(10ng); Blue line: Antigen (50 ng); Red line: Antigen (100 ng);    

  
  

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     Flow cytometric analysis of Hela cells using GAD2 mouse mAb (green) and negative control (red).    

  
  

Glutamic acid decarboxylase 2 (GAD2) antibodies target the 65 kDa isoform of GAD, an enzyme responsible for synthesizing gamma-aminobutyric acid (GABA), the primary inhibitory neurotransmitter in the central nervous system. GAD exists in two isoforms, GAD65 (encoded by GAD2) and GAD67 (encoded by GAD1), with GAD65 predominantly localized to synaptic vesicles in neurons and pancreatic β-cells. GAD2 antibodies are strongly associated with autoimmune disorders, particularly type 1 diabetes mellitus (T1D), where they serve as a key diagnostic marker. Their presence reflects the immune-mediated destruction of pancreatic β-cells, often predating clinical symptoms.

These antibodies are also linked to rare neurological conditions, such as stiff-person syndrome (SPS) and cerebellar ataxia, where they may disrupt GABAergic signaling, leading to motor and cognitive dysfunction. In T1D, GAD2 antibodies are frequently detected alongside other islet autoantibodies (e.g., insulinoma-associated-2 antibodies), aiding in disease classification and risk stratification. Testing for GAD2 antibodies employs immunoassays (e.g., ELISA, RIA) and is critical for distinguishing autoimmune diabetes from type 2 diabetes. Elevated titers may correlate with faster β-cell decline, though their pathogenic role remains debated. Research suggests molecular mimicry or epitope spreading as potential triggers for autoantibody production. Understanding GAD2 antibodies enhances insights into autoimmune mechanisms and informs personalized therapeutic approaches.