Alzheimer′s disease(AD) is one of the most common neurodegenerative diseases,showing progressive memory and cognitive deficits.The predominant neuropathological features of AD are extracellular senile plaques(SP) composed by over expression of amyloid beta protein(Aβ),hyperphosphorylation of Tau protein forming the neurofibrillary tangles(NFTs) and neuronal loss in the specific brain subregions.However,the cause of dementia of AD are still not known,the neurotoxicity of over expressed Aβ coming from the proteolysis of amyloid precursor protein(APP) may play a important role.Aβ neurotoxicity has been widely reported in vitro and in vivo,including the impairment of long term potentiation(LTP),disruption of synaptic plasticity.Aβ also triggered neuron inflammation,and disturbed neurogenesis.caused neuronal oxidative damage and apoptosis,eventually resulted in memory loss At this moment,there are no effective pharmacologic interventions that could halt the progression of AD.Current pharmacotherapies,such as acetylcholinesterase inhibitors including donepezil,rivastigmine and galantamine,and a NMDA antagonist,memantine,improve symptoms but do not block the disease progression.New strategies to slow and/or reverse the pathogenesis of patients with AD are greatly needed.Traditional Chinese Medicine such as icariin may provide an unique opportunity for seeking more safe and effective therapies for AD.In this study we were examine the protective effect of icariin on Tg2576 mice,a well established animal model of AD.Our results demonstrated that chronic treatment of Tg2576 mice with icariin from age of 8 to 11 months,could improve the memory function of Tg2576 mice.In addition,icariin decreased the APP,Aβ levels,and amyloid plaque number in Tg2576 mouse brain.Finally,icariin promoted cell proliferation and differentiation into neuron in the dentate gyrus(DG) of hippocampus in aged Tg2576 mouse.Neurogenesis following icariin administration may due to the decrease of Aβ levels and phosphodiesterase type 5(PDE5),amelioration of the Aβ neurotoxicity,and increase of brain-derived neurotrophic factor(BDNF) expression in mouse brain.In summary,aged Tg2576 mice deministrated neuropathogenesis and cognitive deficits in thebrain,.Chronic treatment of icariin in Tg2576 mice significantly decreased the neuropathogenesis and improved cognitive function.Icariin stimulates neurogenesis in aged Tg2576 mice displayed further neuro-protection in aged brain.Our results provide solid evidence in support that icariin could be a potential compound for AD therapy. Alzheimer’s disease (AD) is one of the most common neurodegenerative diseases, showing progressive memory and cognitive deficits. The predominant neuropathological features of AD are extracellular senile plaques (SP) composed of over expression of amyloid beta protein (Aβ), hyperphosphorylation of Tau protein forming the neurofibrillary tangles (NFTs) and neuronal loss in the specific brain subregions. Despite, the cause of dementia of AD are still not known, the neurotoxicity of over expressed Aβ coming from the proteolysis of amyloid precursor protein (APP) may play a important role. Aβ neurotoxicity has been widely reported in vitro and in vivo, including the impairment of long term potentiation (LTP), disruption of synaptic plasticity. Aβ also triggered neuron inflammation, and disturbed neurogenesis. Caused neuronal oxidative damage and apoptosis, apoptosis resulted in memory loss At this moment, there are no effective pharmacologic interventions that could have halt the progression of AD.Current p harmacotherapies, such as acetylcholinesterase inhibitors including donepezil, rivastigmine and galantamine, and a NMDA antagonist, memantine, improve symptoms but do not block the disease progression .New strategies to slow and / or reverse the pathogenesis of patients with AD are greatly needed.Traditional Chinese Medicine such as icariin may provide an unique opportunity for seeking more safe and effective therapies for AD. In this study we were examined the protective effect of icariin on Tg2576 mice, a well established animal model of AD. Our results demonstrates that chronic treatment of Tg2576 mice with icariin from age of 8 to 11 months, could improve the memory function of Tg2576 mice. In addition, icariin decreased the APP, Aβ levels, and amyloid plaque number in Tg2576 mouse brain. Finally, icariin promoted cell proliferation and differentiation into neuron in the dentate gyrus (DG) of hippocampus in aged Tg2576 mouse. Neurogenesis following icariin administration may due to the decrease of Aβ levelsand phosphodiesterase type 5 (PDE5), amelioration of the Aβ neurotoxicity, and increase of brain-derived neurotrophic factor (BDNF) expression in mouse brain. In summary, aged Tg2576 mice deministrated neuropathogenesis and cognitive deficits in therain, .Chronic treatment of icariin in Tg2576 mice significantly decreased the neuropathogenesis and improved cognitive function. Icariin stimulates neurogenesis in aged Tg2576 mice displayed further neuro-protection in aged brain. These results provide solid evidence in support that icariin could be a potential compound for AD therapy.