RESEARCH ARTICLE Cognitive dysfunction asso o

Full list of author information is available at the end of the articleBackground Glutamic acid decarboxylase (GAD) is the rate-limiting enzyme in the synthesis of γ-aminobutyric acid (GABA), a major inhibitory neurotransmitter that modulates and synchronizes neural network activity in the CNS [1]. Two isoforms of the enzyme, GAD65 and GAD67, are found in the CNS. Autoantibodies (GADA) against GAD65 inhibit the activity of GAD65 and therefore im-pair GABA synthesis. Various neurological manifesta-tions are associated with GADA, including stiff person syndrome (SPS), cerebellar ataxia, epilepsy, and limbic encephalitis [2]. Intrathecal GADA synthesis induces symptoms in the CNS, presumably by affecting the GABAergic system [3], which is involved in cognitive function. However, little is known regarding the relation-ship between GADA and cognitive impairment. Serum GADA play a role in the pathogenesis of th