Neuroinflammatory responses caused by amyloid β(Aβ) play an important role in the pathogenesis of Alzheimers disease (AD).Aβ is known to be directly responsible for the activation of glial cells and induction of apoptosis.Akebia Saponin D (ASD) is extracted from a traditional herbal medicine Dipsacus asper Wall,which has been shown to protect against ibotenic acid-induced cognitive deficits and cell death in rats.In this study,we investigated the protective effect of ASD on learning and memory impairment induced by Aβ1-42 in vivo using morris water and Y-maze task.Furthermore,the anti-inflammatory activity and neuroprotective effect of ASD was examined with methods of histochemistry and biochemistry.These data showed that oral administration with ASD at the doses of 30,90 and 270 mg/kg exerted an improved effect on cognitive impairment.Subsequently,the ASD inhibited the activation of glial cells and the expression of tumor necrosis factor (TNF)-α,interleukin-1 beta (IL-1β) and cyclooxygenase-2 (COX-2) in rat brain.ASD afforded a benefical action on inhibitions of Akt,as well as inhibitions of IκB kinase (IKK) phosphorylation and activation of transcription factors of the nuclear factor κB (NF-κB) produced by Aβ1-42.