Thus, as observed in other models of neurodegenerative disorders such as Alzheimer’s disease [9] and convulsions-induced neuronal damage [30], the role of A2AR is initially designed to facilitate synaptic plasticity in non-diseased conditions; however, A2AR overfunction causes an abnormal increase of synaptic plasticity that seems to contribute to the onset of synaptic damage. The gene discussed is ADORA2A; the disease is Alzheimer disease.