摘要：OBJECTIVE Alzheimer disease(AD) is the most common type of dementia and is featured by the accumulation of β-amyloid peptide(Aβ) in the brain. The Alpha 7 nicotinic acetylcholine receptor family(α7 nAChR) was widely considered to interact with that Aβ, mediate neuroprotection and improve cognitive performance. However, the mechanisms underlying these interactions remain elusive. The present study aimed to determine how this interaction contribute to AD pathology. METHODS In vitro model of AD(primary culture of mice hippocampus treated with Aβ) and in vivo, a mouse model of AD(APPswe/PSEN1 d E9 double transgenic mice, APP/PS1_DT mice) were used to study to the possible inter-action of α7 nAChR and Aβ in the pathogenesis of AD. In vitro experiments, the primary hippocampal neurons cell was exposed to Aβ1-42 peptides in combination with PNU. In vivo experiments, different drugs/operations was applied to APP/PS1_DT mice for setting up of the following groups: WP group, wild-type C57 mice treated with PNU(α7 nAChR specific agonist);AP group, APP/PS1_DT mice treated with PNU;APP/PS1 group, the APP/PS1_DT mice injected intraperitoneally with the same amount of normal saline for 5 d;Control group, wild-type C57 mice injected intraperitoneally with the same amount of normal saline for 5 d. A transmission electron microscope was used to observed the synaptic morphological changes of hippocampal neurons. Reverse transcription quantitative PCR(RT-q PCR) and Western blot analysis were used to detect the expression levels of synaptic-associated proteins(SYN, SNAP25 etc). The learning and memory abilities of mice were detected by Morris water maze. RESULTS In vitro, it was found that α7 nAChR acts as an anti-Aβ-induced synaptic injury to nerve cell by increased the expression of synaptic-associated proteins and attenuated apoptosis induced by Aβ oligomers. In vivo, α7 nAChR attenuated synaptic loss induced by Aβ1-42, reduced the deposition of Aβ1-42 in the hippocampus and maintained the integrity of synaptic stru

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