{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,17]],"date-time":"2026-09-17T06:01:18Z","timestamp":1789624878234,"version":"build-2803163510"},"reference-count":71,"publisher":"Wiley","issue":"9","license":[{"start":{"date-parts":[[2025,5,3]],"date-time":"2025-05-03T00:00:00Z","timestamp":1746230400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["faseb.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["The FASEB Journal"],"published-print":{"date-parts":[[2025,5,15]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    Chronic inflammatory conditions like periodontitis and inflammatory bowel disease (IBD) are reported to contribute to the pathogenesis of late\u2010onset Alzheimer's disease (AD). Gram\u2010negative bacteria are the main bacterial species causing oral and gut mucosal infections. Lipopolysaccharide (LPS) is a major inflammation\u2010inducing molecule in Gram\u2010negative bacteria. LPS derived from the oral bacterium\n                    <jats:styled-content style=\"fixed-case\">\n                      <jats:italic>Porphyromonas gingivalis<\/jats:italic>\n                    <\/jats:styled-content>\n                    exhibits heterogeneous tetra\u2010acylated and penta\u2010acylated lipid A, while LPS from\n                    <jats:styled-content style=\"fixed-case\">\n                      <jats:italic>Escherichia coli<\/jats:italic>\n                    <\/jats:styled-content>\n                    exhibits the classical hexa\u2010acylated lipid A. Whether\n                    <jats:styled-content style=\"fixed-case\">\n                      <jats:italic>P. gingivalis<\/jats:italic>\n                    <\/jats:styled-content>\n                    \u2010LPS and\n                    <jats:styled-content style=\"fixed-case\">\n                      <jats:italic>E. coli<\/jats:italic>\n                    <\/jats:styled-content>\n                    \u2010LPS play a similar role in the progression of late\u2010onset AD is unknown. Using adult, wild\u2010type C57BL\/6J mice to mimic the adult population without genetically determined predisposition to AD, we showed that chronic inflammation induced by a 28\u2010day, subcutaneous infusion of\n                    <jats:styled-content style=\"fixed-case\">\n                      <jats:italic>P. gingivalis<\/jats:italic>\n                    <\/jats:styled-content>\n                    \u2010LPS or\n                    <jats:styled-content style=\"fixed-case\">\n                      <jats:italic>E. coli<\/jats:italic>\n                    <\/jats:styled-content>\n                    \u2010LPS can lead to neuroinflammation and AD\u2010like cognitive decline and pathology in male mice. At this relatively early stage (4\u2009weeks) of chronic inflammation when the blood\u2013brain barrier is intact, both\n                    <jats:styled-content style=\"fixed-case\">\n                      <jats:italic>P. gingivalis<\/jats:italic>\n                    <\/jats:styled-content>\n                    \u2010LPS and\n                    <jats:styled-content style=\"fixed-case\">\n                      <jats:italic>E. coli<\/jats:italic>\n                    <\/jats:styled-content>\n                    \u2010LPS cause neuroinflammation through Toll\u2010like receptor 4 (TLR4) and Toll\u2010like receptor 2 (TLR2) expressed at microglia in the brain. Notably, only\n                    <jats:styled-content style=\"fixed-case\">\n                      <jats:italic>E. coli<\/jats:italic>\n                    <\/jats:styled-content>\n                    \u2010LPS induces significant inflammatory responses systemically. In short, our results suggest that chronic\n                    <jats:styled-content style=\"fixed-case\">\n                      <jats:italic>P. gingivalis<\/jats:italic>\n                    <\/jats:styled-content>\n                    \u2010LPS release (occurring in chronic periodontitis) or\n                    <jats:styled-content style=\"fixed-case\">\n                      <jats:italic>E. coli<\/jats:italic>\n                    <\/jats:styled-content>\n                    \u2010LPS release (occurring in IBD) could harm the brain before the blood\u2013brain barrier is disrupted; continuous local\n                    <jats:styled-content style=\"fixed-case\">\n                      <jats:italic>P. gingivalis<\/jats:italic>\n                    <\/jats:styled-content>\n                    \u2010LPS release might do harm to the brain before exhibiting adverse effects systemically.\n                  <\/jats:p>","DOI":"10.1096\/fj.202403117rr","type":"journal-article","created":{"date-parts":[[2025,5,3]],"date-time":"2025-05-03T06:48:11Z","timestamp":1746254891000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":11,"title":["Chronic Lipopolysaccharide Exposure Causes\n                    <scp>AD<\/scp>\n                    \u2010Like Pathology in Male Mice With Intact Blood\u2013Brain Barrier"],"prefix":"10.1096","volume":"39","author":[{"given":"Fady","family":"Eid","sequence":"first","affiliation":[{"name":"Department of Periodontology Boston University Henry M. 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