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This review synthesizes epidemiological, pathological, and mechanistic evidence underpinning their interconnected pathogenesis.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results and Conclusion<\/jats:title>\n                    <jats:p>\n                      Epidemiologically, periodontitis is associated with an increased risk of AD, while AD patients exhibit a higher prevalence of periodontitis, driven by cognitive decline\u2010impaired oral hygiene and synergistic inflammatory mechanisms. Pathologically, periodontal pathogens (e.g.,\n                      <jats:styled-content style=\"fixed-case\">\n                        <jats:italic>Porphyromonas gingivalis<\/jats:italic>\n                      <\/jats:styled-content>\n                      ) translocate to the brain via hematogenous, trigeminal, or oral\u2010intestinal pathways, inducing neuroinflammation, \u03b2\u2010amyloid (A\u03b2) aggregation, and tau hyperphosphorylation through virulence factors like gingipains and LPS. Conversely, AD\u2010related neurodegeneration disrupts bone homeostasis to aggravate periodontitis via multiple mechanisms: (1) A\u03b2\u2010mediated osteoclast activation through RAGE\/NF\u2010\u03baB signaling and suppression of osteoblastogenesis; (2) autonomic nervous system dysregulation, where sympathetic hyperactivity promotes RANKL\u2010dependent bone resorption; and (3) endocrine dysfunction, including HPA axis hyperactivation (chronic hypercortisolism), sex hormone deficiency, insulin resistance, and growth hormone\/IGF\u20101 insufficiency, all of which perturb the balance between bone formation and resorption. Aging exacerbates this bidirectional interplay through immunosenescence (e.g., impaired neutrophil phagocytosis, senescent microglia) and inflammaging, creating a pro\u2010degenerative milieu that amplifies both diseases. Clinical interventions, such as periodontal therapy and microbiota modulation, show promise in reducing systemic inflammation and slowing AD progression, though causal links require validation. Future research must prioritize longitudinal cohort studies, pathogen\u2010specific mechanistic investigations, and translational strategies targeting the oral\u2010brain axis to develop preventive interventions for aging populations.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/cns.70754","type":"journal-article","created":{"date-parts":[[2026,1,27]],"date-time":"2026-01-27T06:09:00Z","timestamp":1769494140000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":9,"title":["The Interface of Oral and Brain Health: Current Insights Into the Bidirectional Relationship Between Alzheimer's Disease and Periodontitis"],"prefix":"10.1002","volume":"32","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-5680-679X","authenticated-orcid":false,"given":"Weidong","family":"Zhang","sequence":"first","affiliation":[{"name":"Department of Bone Metabolism, School and Hospital of Stomatology, Cheeloo College of 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