Ludewig applied purified patient antibodies to mouse hippocampal slices and found that incubation with anti-LGI1 antibodies derived from patients with non-FBDS seizures and cognitive impairment resulted in a significant decline in long-term potentiation or short-term plasticity at CA3-CA1 neurons, as well as decreased hippocampal synaptic density. The gene discussed is LGI1; the disease is Cognitive impairment.