Hippocampal neurons treated with sera from GAD-positive epileptic patients show increased post-synaptic inhibitory potentials [58, 59], while rat cerebellar slices exposed to serum or CSF from patients with SPS or cerebellar ataxia, exhibit decreased post-synaptic inhibitory currents of Purkinje cells [59]. Here, GAD1 is linked to aceruloplasminemia.