Objective: Microglial inflammation may significantly contribute to the pathology of Alzheimer's disease. To examine the potential of C. cochinchinensis to ameliorate amyloid β protein (Aβ-induced microglia activation, BV-2 and primary glial mixed cultured were employed. Methods: Lipopolysaccharide (LPS), Interferon-y (IFN-y), fibrillary Aβ (fAβ), or oligomeric Aβ (oAβ) were used to activate microglia. LPS and IFN-y, but not Aβs, activated BV-2 cells to produce nitric oxide through an increase in inducible nitric oxide synthase (iNOS) expression without significant effects on cell viability of microglia. fAβ but not oAβ, enhanced the IFN-ystimulated nitric oxide production and iNOS expression. Results: The ethanol/water extracts of C. cochinchinensis (CC-EW) and the purified isolated components (CCA to CCF) effectively reduced the nitric oxide production and iNOS expression stimulated by IFN-y combined with fAβ. oAβ effectively activated the ramified microglia in mixed glial culture by observing the morphological alteration of the microglia from ramified to amoeboid. CC-EW and CCB effectively prohibit the Aβ-mediated morphological change of microglia. CC-EW and CCB effectively promote Aβ clearance. Conclusion: The components of Cudrania cochinchinensis including CC-EW and CCB are potential for novel therapeutic intervention for Alzheimer's disease.