In the CSF the antibodies target more domains of GAD65 and also immunoreact with GAD67, 2) GAD65-ab titres were higher in the CSF of patients with LE or cerebellar ataxia compared to those with SPS, 3) the frequency of additional antibodies against antigens of the GABAergic inhibitory synapses is low across all neurological syndromes, and 4) GAD-ab are not internalized by primary neuronal cultures suggesting that GAD-ab are not directly pathogenic. This evidence concerns the gene GAD2 and aceruloplasminemia.