studies that compared brain neocortex and parietal cortex of postmortem patients with AD to those of the normal aged controls, the low level of P2Y2R expression was associated with neuropathology and synapse loss in patients with AD,263 presenting additional support for neuroprotective function of P2Y2R in AD pathology.264 Additionally, activation of the P2Y2R has shown to promote neurite outgrowth.265 These studies suggest that loss of neuroprotective functions of P2Y2R might contribute to disease pathogenesis in AD, and therefore, targeting the P2Y2Rs with agonist might be a promising strategy to boost neuroprotection in neurodegenerative diseases.
