Immunization against GAD induces antibody binding to GAD-independent antigens and brainstem GABAergic neuronal loss.

We conclude that although immunization with GAD65 did not produce an overt clinical phenotype of SPS in mice and the loss of GABAergic neurons in the brainstem did not quite reach statistical significance, nevertheless these findings suggest an integral role for GAD65 immunity in the pathogenesis of SPS but a role which includes the development of novel cell-surface antibodies which might perhaps begin to provide a basis for the phenotypic diversity.

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