Inflammatory reactions contribute to disease progression and severity of Alzheimer’s disease (AD). While multiple animal studies have suggested that increased neuroinflammation occurs in AD, few studies have investigated neuroinflammation in human subjects. This is the first study using the third-generation TSPO ligand [18F]-GE180 to evaluate the neuroinflammation in AD on human subjects. Our study suggests that neuroinflammation accumulates together with amyloid deposition and reaches a plateau when the regional amyloid SUVR reaches 1.1 threshold. Compared to amyloid pathology, neuroinflammation is more closely related to hyperconnectivity in MCI/AD subjects.