目的：基于微阵列分析筛选阿尔茨海默病（Alzheimer disease，AD）自噬相关基因，并进行通路分析，鉴定关键基因，以期探究潜在的发病机制与治疗靶点。方法：从GEO数据库下载GSE33000数据集，通过R软件limma包获取AD差异表达基因，从人类自噬基因数据库、人类自噬调节因子数据库及GeneCard数据库分别下载自噬相关基因，获得自噬相关基因集，将差异表达基因与自噬相关基因集取交集，获得AD自噬相关基因。使用R软件org.Hs.eg.db、clusterProfiler等程序包进行基因本体论（gene ontology，GO）分析、京都基因和基因组百科全书（Kyoto Encyclopedia of Genes and Genomes，KEGG）分析，利用在线软件STRING进行蛋白互作网络分析，并基于最大团中心性（maximal clique centrality，MCC）算法进行关键基因预测。结果：共获得66个AD自噬相关基因，其中41个基因上调，25个基因下调。基因富集分析显示，GO分析中细胞组分主要富集在吞噬小泡膜、分泌颗粒膜、膜微结构域、晚期内体等，分子功能主要富集在结合Toll样受体、结合泛素连接酶等，生物学过程富集在调节自噬、细胞分解代谢的调节、脂多糖诱导的反应、调节炎症反应、外部刺激的细胞反应等。在KEGG富集分析中，差异表达的自噬相关基因主要富集在NOD样受体信号通路、脂质与动脉粥样硬化、叉头框蛋白O（forkhead box protein O，FoxO）信号通路等。完成蛋白互作网络（protein-protein interaction，PPI）的构建，同时鉴定出10个关键基因，筛选出与AD关联较大的为白介素-6（interleukin -6，IL-6）、信号转导与转录激活因子3(signal transducer and activator of transcription 3, STAT3)。结论：本研究获得10个关键ADARG，其中与AD关联较大的为IL-6、STAT3。

Objective Screen autophagy related genes of Alzheimer disease(AD) based on microarray analysis, conduct pathway analysis and identify key genes in order to explore potential pathogenesis and therapeutic targets. Methods The GSE33000 dataset was downloaded from GEO Database, and the differentially expressed genes of AD were obtained by R software limma package. Autophagy-related genes were downloaded from Human Autophagy Database, Human Autophagy Modulator Database and GeneCard Database, respectively, and the autophagy-related gene set was obtained. The AD autophagy-related genes were obtained through intersecting the differentially expressed genes with the autophagy-related gene set. The R software packages such as org.Hs.eg.db and clusterProfiler were used to perform gene ontology (GO) analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis, the online software Search Tool for the Retrieval of Interacting Genes (STRING) was used to conduct protein-protein interaction network analysis, and the key genes were predicted based on MCC algorithm. Results A total of 66 autophagy related genes were obtained, of which 41 genes were up-regulated and 25 genes were down-regulated. Gene enrichment analysis showed that cellular components in GO analysis were mainly enriched in phagocytic vesicle membrane, secretory granule membrane, membrane microdomain, late endosome, etc., and molecular functions were mainly enriched in Toll-like receptor binding, ubiquitin-like protein ligase binding, etc., and biological processes were enriched in regulation of autophagy, positive regulation of cellular catabolic process, response to lipopolysaccharide, regulation of inflammatory response, cellular response to external stimulus, etc. In KEGG enrichment analysis, the differentially expressed autophagy-related genes were mainly concentrated in NOD-like receptor signaling pathway, lipid and atherosclerosis, forkhead box protein O(FoxO) signaling pathway, etc. Our research completed the construction of protein-protein interaction (PPI), identified 10 key genes, and screened out that interleukin-6(IL-6) and signal transducer and activator of transcription 3(STAT3) were closely related to AD. Conclusions Ten key autophagy-related genes were obtained in this study, among which IL-6 and STAT3 are more closely related to AD.