SNCA and Parkinson disease: Accordingly, A53T mice overexpressing mutant α-synuclein displayed a significant increase in reactive astrocytes and increased production of ROS and proinflammatory prostaglandins such as cyclooxygenase 1 (COX-1) as compared to WT, suggesting that accumulation of α-synuclein leads to neuroinflammation, reactive astrogliosis, and consequent PD pathogenesis [94].