Likewise, in AD mice and in aged mice, a cortical and hippocampal upsurge of A2AR was reported mainly in glutamatergic synapses (Diógenes et al., 2007; Canas et al., 2009; Costenla et al., 2011), and recently, A2AR overexpression was reported to be sufficient to drive age-like memory impairments in young rats and to uncover a hippocampal LTD-to-LTP shift, which is a signature of memory impairment (Temido-Ferreira et al., 2020). The gene discussed is ADORA2A; the disease is memory impairment.