After all, accumulating evidence implicates dysregulated adenosine metabolism in many neurodegenerative diseases; for example, an up-regulation of ADA, ADK and CD73 has been found both in patients and in mouse models of Alzheimer’s disease (AD) [25,27,28,29]; ENT1, ENT2 and ADA were found increased in Huntington’s disease (HD) [16]. Here, SLC29A2 is linked to juvenile Huntington disease.