Abstract.
Glutamic acid decarboxylase (GAD) is the enzyme that catalyses the production of GABA, a major neurotransmitter of the central nervous system. Antibodies to GAD (GAD-Ab) were first recognised in a patient affected by stiff-person syndrome; subsequently they were reported in a large number of cases with type 1 diabetes. Recently GADAb have been described in a number of patients affected by chronic cerebellar ataxia, drug-resistant epilepsy and myoclonus. These cases usually harbour other autoantibodies or are affected by organ-specific autoimmune diseases. The role of GAD-Ab is still unclear; the lack of experimental models makes it difficult to investigate their potential pathogenetic role. However two mechanisms have been suggested: the reduction by GAD-Ab of GABA synthesis in nerve terminals or the interference with exocytosis of GABA.
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Received: 16 May 2002 / Accepted in revised form: 10 July 2002
Correspondence to B. Giometto
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Vianello, M., Tavolato, B. & Giometto, B. Glutamic acid decarboxylase autoantibodies and neurological disorders. Neurol Sci 23, 145–151 (2002). https://doi.org/10.1007/s100720200055
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DOI: https://doi.org/10.1007/s100720200055