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In this perspective, we explore the hypothesis that a primarily infection\u2010caused chronic dysregulation and weakening of human innate immunity via the underexpression, degradation, and inactivation of innate immune proteins necessary for direct antimicrobial effects and regulation of host defense and autophagy could lead to AD. Key evidence relates to the fact that important innate immune proteins such as LL\u201037\u2014which can bind A\u03b2 and block amyloid formation\u2014as well as Apolipoprotein E, antiviral interferons, and TNF\u2010\u03b1\u00a0can be degraded and deactivated by enzymes produced by the common oral anaerobic pathogen\n                    <jats:italic>Porphyromonas gingivalis<\/jats:italic>\n                    (\n                    <jats:italic>Pg<\/jats:italic>\n                    ).\n                    <jats:italic>Pg<\/jats:italic>\n                    produces numerous virulence factors; of particular importance for AD are\n                    <jats:italic>Pg<\/jats:italic>\n                    \u2019s gingipain cysteine proteases. Deleterious effects of chronic\n                    <jats:italic>Pg<\/jats:italic>\n                    infection and gingipains include a systemic downregulation and paralysis of the interferon response, particularly the antiviral interferon\u2010lambda response, which enables replication of endemic herpesviruses. The result is a chronic, low\u2010level viral infectious assault on gut, nerves, and brain causing the production of A\u03b2 antimicrobial peptides, accumulation of A\u03b2 plaques, phosphorylation of Tau, progressive neuroinflammation, and neurodegeneration. The resultant innate immune system dysregulation, as an AD etiology, ties together the well\u2010known amyloid cascade hypothesis and the infectious theory of AD into a unified explanation of the pathology and cause of AD. If this theory holds true, it suggests preventative approaches: (1) test for and eradicate\n                    <jats:italic>Pg<\/jats:italic>\n                    from oral flora, and\/or directly deactivate the gingipains; and (2) reduce Herpesvirus exacerbations by the use of antiviral drugs and\/or vaccines (e.g., Bacillus Calmette\u2013Gu\u00e9rin).\n                  <\/jats:p>","DOI":"10.1111\/joim.70060","type":"journal-article","created":{"date-parts":[[2025,12,22]],"date-time":"2025-12-22T10:15:39Z","timestamp":1766398539000},"page":"328-348","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":4,"title":["The dysregulation of innate immunity by\n                    <i>Porphyromonas gingivalis<\/i>\n                    in the etiology of Alzheimer's disease"],"prefix":"10.1111","volume":"299","author":[{"given":"Annelise E.","family":"Barron","sequence":"first","affiliation":[{"name":"Department of Bioengineering Schools 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