GAD2 and aceruloplasminemia: In GAD-related gastrointestinal dysmotility hypothetically, antibodies may hinder the conversion of GAD-65 into glutamic acid to GABA, which is expressed in GABAergic nerve terminals in the enteric nervous system.9,12 GAD antibodies were also reported in patients with myasthenia gravis, Lambert-Eaton syndrome, autoimmune dysautonomias, autoimmune encephalopathies, and cerebellar ataxia.8