Adenosine receptors undergo different activities during neurodegeneration progression.66 While both A1 and A2A receptors have shown upregulation in the frontal cortex,67 the A1R expression was reduced in hippocampus, specifically in dentate gyrus, and in CA1, but not in CA3 region.68 Additionally, studies of brain of patients with AD have revealed reduction of striatal A1Rs in this population.31 Several studies have shown that both A1R and A2AR may be involved in metabolism of amyloid β (Aβ) protein and A1 agonists and A2A antagonists might serve as an effective therapy for treating patients with AD.69,70 Moreover, there are some evidences that support the cross talk between A1Rs and A2ARs in other age-related disorders.71-73
