The development and complicacy of Alzheimers disease(AD)are of considerable attribution to the inflammation in brain which is characterized by various up-regulated inflammatory cytokines,especially in response to amyloid β(Aβ).Our aim is to find out the cascade reaction of the high expression of interleukin 23(IL23)and interleukin 17(IL17),which play key role in the pathology of other chronical inflammation diseases,in APP/PS1 Alzheimers disease mouse model and to ensure their feature as a proinflammatory actor effectively disturbing the survive and Aβ cumulation in neuron as well as glia cells(particularly microglia and astrocyte).The expression of IL23 and IL17 was evaluated in APP/PS1 and WT mouse via Solexa mRNA-Seq and QPCR,showed an over-1.5 fold change in mRNA level.Our preliminary research demonstrated that high expression of IL23 and IL17 induced by Aβ in glia cells in vitro,be they primary cultural glia cells(both microglia and astrocyte)or the microglia cell line(BV2)resulted in increasing proliferation of glia cells(need more compact evidences)and suggestively promoted the producing of APP in neuron contributing to the development of AD.We are hopefully waiting to get some positive suggestions from our later hybrids of L23R/IL17R knock-out mouse and APP/PS-1 mouse model.