Neuroinflammation has been observed in post-mortem Alzheimer's disease (AD) brains which could be due to A beta interacting with microglia and astrocytes. SLOH, a carbazole-based fluorophore, was shown to bind to A beta peptides. Herein, we investigated the anti-neuroinflammatory effects of SLOH using a BV-2 microglial cell model and a triple transgenic AD (3xTg-AD) mouse model. BV-2 cells were incubated with A beta in the presence of SLOH for 24 h. The levels of pro-inflammatory and anti-inflammatory cytokines were determined. Moreover, 3xTg-AD mice were administrated with SLOH (2 mg kg(-1)) for one month. The mice were then sacrificed and the brains were used to assess the levels of pro-inflammatory, anti-inflammatory cytokines and the activation of ionized calcium-binding adapter molecule 1 (Iba1). BV-2 cell studies suggested that SLOH reduced the production and mRNA levels of pro-inflammatory cytokines TNF-alpha, IL-1 beta, COX-2, iNOS, and increased IL-10. Animal study confirmed that SLOH reduced the production of pro-inflammatory cytokines and increased the level of anti-inflammatory cytokine. Moreover, SLOH inhibited the activity of GSK-3 beta. In 3xTg-AD mouse model, SLOH treatment significantly decreased the number of Ibal-positive cells in mouse brains. Our results demonstrated that SLOH significantly attenuated the neuroinflammation through down-regulating the activity of GSK-3 beta.