However, it has not yet been tested if the blockade of ecto-5′-nucleotidase or CD73, the rate-limiting ecto-nucleotidase controlling ATP-derived adenosine formation [30,31], is responsible for the engagement of amygdala A2AR in controlling fear memory processing, as it is observed in the hippocampus to control spatial memory deficits in animal models of Alzheimer’s disease [25] or in the striatum to control motor dysfunction in animal models of Parkinson’s disease [32]. This evidence concerns the gene NT5E and Parkinson disease.