摘要Impaired hippocampal neurogenesis is one of the early pathological features of Alzheimer’s disease. Enhancing adult hippocampal neuro-genesis has been pursued as a potential therapeutic strategy for Alzheimer’s disease. Recent studies have demonstrated that environmental novelty activates β2-adrenergic signaling and prevents the memory impairment induced by amyloid-β oligomers. Here, we hypothesized that β2-adrenoceptor activation would enhance neurogenesis and ameliorate memory deifcits in Alzheimer’s disease. To test this hypothe-sis, we investigated the effects and mechanisms of action of β2-adrenoceptor activation on neurogenesis and memory in amyloid precursor protein/presenilin 1 (APP/PS1) mice using the agonist clenbuterol (intraperitoneal injection, 2 mg/kg). We found that β2-adrenoceptor ac-tivation enhanced hippocampal neurogenesis, ameliorated memory deifcits, and increased dendritic branching and the density of dendritic spines. hTese effects were associated with the upregulation of postsynaptic density 95, synapsin 1 and synaptophysin in APP/PS1 mice. Furthermore, β2-adrenoceptor activation decreased cerebral amyloid plaques by decreasing APP phosphorylation at hTr668. hTese ifndings suggest that β2-adrenoceptor activation enhances neurogenesis and ameliorates memory deifcits in APP/PS1 mice.