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Despite the reliance of\n                      <jats:italic toggle=\"yes\">P. gingivalis<\/jats:italic>\n                      on its biofilm for its survival and virulence, the impact of the extracellular matrix on AD\u2019s neuropathological hallmarks has never been examined. In this study, we report a bidirectional relationship between the amyloid-beta (A\u03b2) peptide, which plays a central role in AD, and the biofilm of\n                      <jats:italic toggle=\"yes\">P. gingivalis<\/jats:italic>\n                      . Using multiple fluorescent markers for biofilm components, we observed that A\u03b2\n                      <jats:sub>1-40<\/jats:sub>\n                      inhibited biofilm formation while A\u03b2\n                      <jats:sub>1-42<\/jats:sub>\n                      increased extracellular matrix production. Also, using thioflavin T staining and atomic force microscopy, we observed co-aggregation of the biofilm and monomeric A\u03b2\n                      <jats:sub>1-40<\/jats:sub>\n                      , resulting in faster aggregation and significant changes in aggregate structure. Our findings propose mechanistic explanations for the role of\n                      <jats:italic toggle=\"yes\">P. gingivalis<\/jats:italic>\n                      as a risk factor for AD and offer potential mechanisms for microbial involvement in AD etiology.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>IMPORTANCE<\/jats:title>\n                    <jats:p>\n                      While the etiology of Alzheimer\u2019s disease has been studied extensively for the past 50 years, its exact causes remain unknown. Our current understanding is that the accumulation of multiple genetic and environmental risk factors would lead to the onset of the disease.\n                      <jats:italic toggle=\"yes\">Porphyromonas gingivalis<\/jats:italic>\n                      is a bacterium that produces biofilm and elicits periodontitis, a chronic infection of the gums that constitutes a risk factor for Alzheimer\u2019s disease. While studies have looked at the effects of\n                      <jats:italic toggle=\"yes\">P. gingivalis<\/jats:italic>\n                      in triggering Alzheimer\u2019s symptoms in animal models, none have explored the impact of the biofilm, which is essential in this bacterium. Our study seeks to bridge that gap by demonstrating a bidirectional relationship between\n                      <jats:italic toggle=\"yes\">P. gingivalis<\/jats:italic>\n                      biofilm and amyloid beta, one of the brain lesions involved in Alzheimer\u2019s disease. By understanding the risk factors involved in Alzheimer\u2019s disease and their impact, we aim to provide valuable insights on prevention and treatment.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1128\/spectrum.01981-25","type":"journal-article","created":{"date-parts":[[2026,1,16]],"date-time":"2026-01-16T15:51:48Z","timestamp":1768578708000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":1,"title":["Bidirectional relationship between the biofilm of\n                    <i>Porphyromonas gingivalis<\/i>\n                    and the amyloid-beta peptide"],"prefix":"10.1128","volume":"14","author":[{"given":"David","family":"Dumoulin","sequence":"first","affiliation":[{"name":"D\u00e9partement de Biologie, Universit\u00e9 de Sherbrooke","place":["Sherbrooke, Canada"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mnar","family":"Ghrayeb","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/03qxff017","id-type":"ROR","asserted-by":"publisher"}],"name":"Institute of Chemistry, The Hebrew University of Jerusalem","place":["Jerusalem, Israel"]},{"name":"The Harvey M. 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