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Micro\u2010computed tomography (Micro\u2010CT) was used to observe the destruction of the alveolar bone. Nested quantitative polymerase chain reaction (qPCR) was used to measure small quantities of <jats:italic>P.gingivalis<\/jats:italic> DNA in different tissues. Behavioral experiments were performed to measure cognitive function in the mice. The mRNA levels of <jats:italic>TNF\u2010\u03b1<\/jats:italic>, <jats:italic>IL\u20106<\/jats:italic>, <jats:italic>IL\u20108<\/jats:italic>, <jats:italic>RANKL<\/jats:italic>, <jats:italic>OPG<\/jats:italic>, <jats:italic>APP695<\/jats:italic>, <jats:italic>APP751<\/jats:italic>, <jats:italic>APP770<\/jats:italic>, and <jats:italic>BACE1<\/jats:italic> in the gingival tissues or cortex were detected by RT\u2010PCR. The levels of A\u03b21\u201040 and A\u03b21\u201042 in gingival crevicular fluid (GCF) and plasma were tested by ELISA.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p><jats:italic>P.\u2009gingivalis<\/jats:italic> oral infection was found to cause alveolar bone resorption and impaired learning and memory. <jats:italic>P.gingivalis<\/jats:italic> DNA was detected in the gingiva, blood and cortex of the <jats:italic>P.gingivalis<\/jats:italic> group by nested qPCR (<jats:italic>p<\/jats:italic>\u2009&lt;\u2009.05). The mRNA expression of <jats:italic>TNF\u2010\u03b1<\/jats:italic>, <jats:italic>IL\u20106<\/jats:italic>, <jats:italic>IL\u20108<\/jats:italic>, <jats:italic>RANKL\/OPG<\/jats:italic>, and <jats:italic>BACE1<\/jats:italic> in the gingival tissue was significantly higher than that in the control group (<jats:italic>p<\/jats:italic>\u2009&lt;\u2009.05). Similarly, upregulated mRNA levels of <jats:italic>APP695<\/jats:italic> and <jats:italic>APP770<\/jats:italic> were observed in the gingival tissuses and cortex of the <jats:italic>P.\u2009gingivalis<\/jats:italic> group (<jats:italic>p<\/jats:italic>\u2009&lt;\u2009.05). The levels of A\u03b21\u201040 and A\u03b21\u201042 in the GCF and plasma of the <jats:italic>P.\u2009gingivalis<\/jats:italic> group were significantly higher than those in the control group (<jats:italic>p<\/jats:italic>\u2009&lt;\u2009.05).<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p><jats:italic>P.\u2009gingivalis<\/jats:italic> can directly invade the brain via hematogenous infection. The invasion of <jats:italic>P.\u2009gingivalis<\/jats:italic> could trigger an immune response and lead to an imbalance between A\u03b2 production and clearance in peripheral tissues, which may trigger an abnormal A\u03b2 metabolite in the brain, resulting in the occurrence and development of AD.<\/jats:p><\/jats:sec>","DOI":"10.1111\/jre.13224","type":"journal-article","created":{"date-parts":[[2024,2,5]],"date-time":"2024-02-05T03:39:11Z","timestamp":1707104351000},"page":"395-407","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":14,"title":["Abnormal amyloid precursor protein processing in periodontal tissue in a murine model of periodontitis induced by <i>Porphyromonas gingivalis<\/i>"],"prefix":"10.1111","volume":"59","author":[{"given":"Hui","family":"Shen","sequence":"first","affiliation":[{"name":"Department of Periodontology Shanghai Ninth People's Hospital Shanghai Jiao Tong University School of Medicine College of 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