{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,7]],"date-time":"2026-10-07T13:00:50Z","timestamp":1791378050682,"version":"4.3.2"},"reference-count":72,"publisher":"Wiley","license":[{"start":{"date-parts":[[2026,10,7]],"date-time":"2026-10-07T00:00:00Z","timestamp":1791331200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,10,7]],"date-time":"2026-10-07T00:00:00Z","timestamp":1791331200000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["bpspubs.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["British J Pharmacology"],"abstract":"<jats:sec>\n                    <jats:title>Background and Purpose<\/jats:title>\n                    <jats:p>Modifying the brain\u2013gut\u2013microbiota axis has emerged as a promising therapeutic strategy against Alzheimer's disease (AD). Whether rifaximin, a non\u2010absorbed and non\u2010systemic antibiotic, can be applied to the treatment of AD remains unexplored. In this study, we investigated the effects of rifaximin using a APP\/PS1 double\u2010transgenic mouse model of AD.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Experimental Approach<\/jats:title>\n                    <jats:p>\n                      Six\u2010month\u2010old male APP\/PS1 mice were administered saline or rifaximin (100\u2009mg\u00b7kg\n                      <jats:sup>\u22121<\/jats:sup>\n                      ) via oral gavage for 2\u00a0months. Gut microbiota composition and metabolites were subsequently analysed to elucidate the underlying mechanisms of rifaximin in AD.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Key Results<\/jats:title>\n                    <jats:p>\n                      Rifaximin modified gut microbiota composition, increasing abundance of\n                      <jats:styled-content style=\"fixed-case\">\n                        <jats:italic>Akkermansia muciniphila<\/jats:italic>\n                      <\/jats:styled-content>\n                      and\n                      <jats:italic>Christensenellaceae<\/jats:italic>\n                      , while decreasing abundance of\n                      <jats:italic>Clostridia_UCG\u2010014<\/jats:italic>\n                      ,\n                      <jats:italic>Muribaculaceae<\/jats:italic>\n                      ,\n                      <jats:italic>Lachnospiraceae<\/jats:italic>\n                      ,\n                      <jats:italic>Turicibacter<\/jats:italic>\n                      ,\n                      <jats:italic>Eubacterium_xylanophilum_group<\/jats:italic>\n                      ,\n                      <jats:italic>Alistipes<\/jats:italic>\n                      ,\n                      <jats:italic>Bacteroides_acidifaciens<\/jats:italic>\n                      and\n                      <jats:italic>Eubacterium_brachy<\/jats:italic>\n                      groups. Furthermore, rifaximin alleviated memory impairment in APP\/PS1 mice, decreased amyloid\u2010\u03b2 (A\u03b2) burden and secondary neuroinflammation and attenuated neuronal death and synaptic dysfunction. Metabolomic analysis revealed that rifaximin altered the profile of gut bile acids by decreasing the concentrations of primary (cholic acid and taurocholic acid) and secondary (taurodeoxycholic acid and taurolithocholic acid) bile acids. Additionally, rifaximin enhanced tryptophan metabolism, shown by increased serum 5\u2010HT concentrations. Both microbial and metabolic shifts were closely correlated with gut microbiota composition.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions and Implications<\/jats:title>\n                    <jats:p>Our results showed that rifaximin alleviated spatial working and short\u2010term recognition memory impairment and mitigated Alzheimer's\u2010like pathological changes in APP\/PS1 mice, effects accompanied by alterations in the gut microbiota\u2013intestinal bile acid profile\u2013serum metabolites network. Rifaximin could provide a new therapeutic approach to the treatment of AD.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/bph.70643","type":"journal-article","created":{"date-parts":[[2026,10,7]],"date-time":"2026-10-07T12:07:27Z","timestamp":1791374847000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Rifaximin ameliorates memory impairment and Alzheimer's pathological changes in APP\/PS1 mice associated with changes in the gut microbiome\u2013bile acids\u2013serum metabolites networks"],"prefix":"10.1111","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-2909-2098","authenticated-orcid":false,"given":"Di","family":"Wu","sequence":"first","affiliation":[{"name":"Department of Neurology Minhang Hospital, Fudan University  Shanghai 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