Abstract: Neuroinflammation, the inflammatory response of the central nervous system (CNS), is a common feature of many neurological disorders such as sepsis-associated encephalopathy (SAE), multiple sclerosis (MS), and Parkinson’s disease (PD). Prior studies identified cytokines (e.g., tumor necrosis factor [TNF], interleukin [IL]-1, and IL-6) delivered by resident glial cells and brain-invading peripheral immune cells as the major contributor to neuroinflammation (Becher et al., 2017). In addition to pro-inflammatory cytokines, elevated levels of extracellular purine molecules such as adenosine triphosphate (ATP) and adenosine can be detected upon any pathological insults (e.g., injury, ischemia, and hypoxia), contributing to the progression of neurological disorders (Borea et al., 2017).