Amyloid plaques in the extracellular parenchyma consist mainly of amyloid-β peptides (Aβ), one of the pathological hallmarks in Alzheimers disease (AD).In the present study, we investigated neuro-inflammation, amyloidogenesis, cognitive impairment following intracerebral injections of Leukotriene D4 (LTD4) in mice.The results demonstrated that LTD4 produced memory impairment and formation of Aβ1-40 and Aβ1-42 both in vivo and in vitro, which were blocked by pranlukast, a cysteinyl leukotriene receptor 1 (CysLT1R) antagonist.In addition, LTD4 increased levels of CysLT1R expression, which was also blocked by pranlukast.These results suggest that LTD4 plays an important role in the mediation of cognitive impairment and amyloidosis associated with AD via CysLT1 receptors, which may be a novel target for treatment of AD.