In fact, during presymptomatic PD, there was an increased A2AR-mediated modulation of corticostriatal LTP driven by an increased synaptic release of ATP without alteration of the density of CD73 and of A2AR. In contrast, upon symptomatic PD, there was an increased density of CD73 and of A2AR now contributing to a reduced corticostriatal LTP magnitude driven by ATP-derived adenosine. The gene discussed is NT5E; the disease is Parkinson disease.