As documented above, regardless of if the worsening pathology is due to altered APP processing, triggered tau hyperphosphorylation and synapse loss or NMDA receptor dysfunction, the potentiation of ROS production and neuroinflammation seem to be calcium-dependent processes, suggesting that imbalanced calcium homeostasis may be a key factor in the aggravation of AD pathology by the diabetic condition. The gene discussed is APP; the disease is Alzheimer disease.