@article{2998749, title = "GAD65 epitope mapping and search for novel autoantibodies in GAD-associated neurological disorders", author = "Fouka, P. and Alexopoulos, H. and Akrivou, S. and Trohatou, O. and Politis, P.K. and Dalakas, M.C.", journal = "Journal of Neuroimmunology", year = "2015", volume = "281", pages = "73-77", publisher = "Elsevier B.V.", issn = "0165-5728", doi = "10.1016/j.jneuroim.2015.03.009", keywords = "anticonvulsive agent; epitope; glutamate decarboxylase 65; glutamate decarboxylase 65 antibody; steroid; autoantibody; glutamate decarboxylase; glutamate decarboxylase 2, adult; animal cell; animal tissue; antibody detection; antibody specificity; Article; brain nerve cell; cerebellar ataxia; clinical article; controlled study; embryo; encephalitis; epilepsy; epitope mapping; female; hippocampus; human; human cell; male; mouse; neurologic disease; nonhuman; pathogenicity; phenotype; priority journal; stiff man syndrome; animal; blood; cell culture; epitope mapping; HEK293 cell line; metabolism; nerve cell; Nervous System Diseases; procedures, Animals; Autoantibodies; Cells, Cultured; Epitope Mapping; Glutamate Decarboxylase; HEK293 Cells; Humans; Mice; Nervous System Diseases; Neurons", abstract = "Antibodies against Glutamic-acid-decarboxylase (GAD65) are seen in various CNS excitability disorders including stiff-person syndrome, cerebellar ataxia, encephalitis and epilepsy. To explore pathogenicity, we examined whether distinct epitope specificities or other co-existing antibodies may account for each disorder.The epitope recognized by all 27 tested patients, irrespective of clinical phenotype, corresponded to the catalytic core of GAD. No autoantibodies against known GABAergic antigens were found. In a screen for novel specificities using live hippocampal neurons, three epilepsy patients, but no other, were positive. We conclude that no GAD-specific epitope defines any neurological syndrome but other antibody specificities may account for certain phenotypes. © 2015 Elsevier B.V." }