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Demographic and cognitive data were collected, and HP infection was confirmed by\n                      <jats:sup>13<\/jats:sup>\n                      C-urea breath test. The levels of BBB variables, neuroinflammatory factors, and AD biomarkers in cerebrospinal fluid (CSF) were measured using enzyme-linked immunosorbent assay. Gut microbiota and metabolites were profiled by 16S ribosomal ribonucleic acid gene sequencing and gas chromatography\u2013mass spectrometry. Correlations and linear regression among above variables were analyzed.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      AD-HP group exhibited impaired overall cognition and cognitive domains of immediate and short-term memory and language, and elevated CSF levels of matrix metallopeptidase (MMP) 9, vascular endothelial growth factor (VEGF), interferon-\u03b3, and phosphorylated tau (P-tau) 181. Overall cognitive score was positively correlated with amyloid-\u03b2\n                      <jats:sub>42<\/jats:sub>\n                      and negatively with P-tau181 levels in CSF. Positive correlations were observed between P-tau181 and soluble triggering receptor expressed on myeloid cells 2, between P-tau231 and chitinase-3-like protein, and between P-tau231 and BBB variables (receptor for advanced glycation endproducts, MMP9, zsonula occludens-1, and claudin-5). In AD-HP group, there was a unique dysbiosis pattern of gut microbiota and metabolites, and HP was particularly associated with the reduced gut 23-nordeoxycholic acid methyl ester and elevated CSF VEGF level (all p\u2009&lt;\u20090.05).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>HP infection exacerbates gut dysbiosis, promotes BBB disruption, intensifies neuroinflammation, accelerates AD pathology, and aggravates cognitive decline.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1177\/13872877251412234","type":"journal-article","created":{"date-parts":[[2026,1,27]],"date-time":"2026-01-27T10:57:23Z","timestamp":1769511443000},"page":"1633-1648","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":6,"title":["The roles of helicobacter pylori infection on the pathogenesis of Alzheimer's disease: Gut-brain axis dysfunction and blood-brain barrier disruption"],"prefix":"10.1177","volume":"109","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-4025-1061","authenticated-orcid":false,"given":"Jing","family":"Li","sequence":"first","affiliation":[{"name":"Department of Neurology, Beijing Tiantan Hospital, Capital Medical University, Beijing, China"},{"name":"Center for Cognitive Neurology, Department of Neurology, Beijing Tiantan Hospital, Capital Medical University, Beijing, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0006-9240-3393","authenticated-orcid":false,"given":"Hao","family":"Yue","sequence":"additional","affiliation":[{"name":"Department of Neurology, Beijing Tiantan Hospital, Capital Medical University, Beijing, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tenghong","family":"Lian","sequence":"additional","affiliation":[{"name":"Center for Cognitive Neurology, Department 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