Article(id=1280817525692805295, tenantId=1146029695717560320, journalId=1192105938417971205, issueId=1280817479555462000, articleNumber=null, orderNo=null, doi=10.13343/j.cnki.wsxb.20250916, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=research-article, receivedDate=1765123200000, receivedDateStr=2025-12-08, revisedDate=null, revisedDateStr=null, acceptedDate=1773676800000, acceptedDateStr=2026-03-17, onlineDate=1783300294564, onlineDateStr=2026-07-06, pubDate=1783094400000, pubDateStr=2026-07-04, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1783300294564, onlineIssueDateStr=2026-07-06, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1783300294564, creator=13701087609, updateTime=1783300294564, updator=13701087609, issue=Issue{id=1280817479555462000, tenantId=1146029695717560320, journalId=1192105938417971205, year='2026', volume='66', issue='7', pageStart='3121', pageEnd='3677', issueExtLink='null', onlineDate='null', pubDate='1783094400000', pubDateStr='2026-07-04', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=1, specialIssue=null, createTime=1783300283564, creator='13701087609', updateTime=1783326087324, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1280925708813832745, tenantId=1146029695717560320, journalId=1192105938417971205, issueId=1280817479555462000, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1280925708813832746, tenantId=1146029695717560320, journalId=1192105938417971205, issueId=1280817479555462000, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=3139, endPage=3149, ext={EN=ArticleExt(id=1280817529471873201, articleId=1280817525692805295, tenantId=1146029695717560320, journalId=1192105938417971205, language=EN, title=Research progress in the role of key metabolites of gut microbiota in the progression of Alzheimer’s disease, columnId=1192149543727808575, journalTitle=Acta Microbiologica Sinica, columnName=Review, runingTitle=null, highlight=null, articleAbstract=

Alzheimer’s disease (AD) is a complex neurodegenerative disorder characterized by progressive cognitive impairment. In recent years, the “gut-brain axis” has been recognized to play an important role in the pathogenesis of AD, with the gut microbiota-derived metabolites serving as key mediators of gut-brain communication. This review systematically summarizes the alterations and underlying molecular mechanisms of five classes of key metabolites—short-chain fatty acids, bile acids, indole derivatives, trimethylamine N-oxide, and lipopolysaccharides—during the progression of AD. This review not only provides new perspectives for understanding the pathological processes of AD but also lays a theoretical foundation for the development of diagnostic and therapeutic strategies based on microbiota modulation.

, authors=Jianxing ZHENG^{1, 2}, Mengqing ZHAO³, Yunchen LUO², Tiegang XIAO², Yueshuang ZHAO⁴, Shuqing ZHAO³, Jun XU², Bing WANG², authorsList=Jianxing ZHENG, Mengqing ZHAO, Yunchen LUO, Tiegang XIAO, Yueshuang ZHAO, Shuqing ZHAO, Jun XU, Bing WANG, authorCompany=null, correspAuthors=Jun XU, Bing WANG, authorNote=, correspAuthorsNote=, copyrightStatement=null, copyrightOwner=null, extLink=null, articleAbsUrl=null, sourceXml=null, magXml=null, pdfUrl=null, pdf=null, pdfFileSize=null, pdfExtLink=null, richHtmlUrl=null, mobilePdfUrl=null, reviewReport=null, pdfFirstPage=null, abstractGraph=null, abstractGraphContent=null, abstractVideo=null, citation=null, cebUrl=null, magXmlContent=null, mapNumber=null, fund=null), CN=ArticleExt(id=1280817530147156148, articleId=1280817525692805295, tenantId=1146029695717560320, journalId=1192105938417971205, language=CN, title=肠道菌群关键代谢物对阿尔茨海默病进程的研究进展, columnId=1192149543882997826, journalTitle=微生物学报, columnName=综述, runingTitle=null, highlight=null, articleAbstract=

阿尔茨海默病(Alzheimer’s disease, AD)是一种以进行性认知障碍为特征的复杂神经退行性疾病。近年来，“肠-脑轴”在AD的发病机制中发挥重要作用，而肠道菌群来源的代谢物是肠脑通信的关键媒介。本文围绕短链脂肪酸(short-chain fatty acids, SCFAs)、胆汁酸(bile acids, BAs)、吲哚类代谢物、三甲胺-N-氧化物(trimethylamine N-oxide, TMAO)和脂多糖(lipopolysaccharides, LPS)这5类关键代谢物，系统总结其在AD进程中的变化及其分子机制。这不仅为理解AD病理进程提供了新视角，也为开发基于菌群干预的诊断与治疗策略奠定了理论基础。

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