Furthermore, in animal models of temporal lobe epilepsy [42] and of Parkinson’s disease [45], A2AR overfunction predates alterations of synaptic plasticity and of behavior that are characteristic of these diseases, prompting the hypothesis that A2AR upregulation might actually be a trigger of brain dysfunction resulting from aberrant synaptic plasticity [46]. The gene discussed is ADORA2A; the disease is Parkinson disease.