Based on the clinical findings of late-onset temporal lobe epilepsy with a pharmacoresistant course, impairment of both, verbal and nonverbal declarative memory, a slight increase of signal intensity in the right amygdala without hippocampal atrophy or sclerosis and high GAD65 and positive GAD67 antibodies in serum and CSF, a GAD antibody-associated limbic encephalitis was diagnosed. This evidence concerns the gene GAD1 and hippocampal atrophy.