PBT2 can kill bacteria but so can perhaps also ATH434 as it is an iron chelator and pyrphyromonas gingivalis needs iron???

Crit Rev Microbiol

. 2023 Jan 4;1-11.

doi: 10.1080/1040841X.2022.2163613. Online ahead of print.

Porphyromonas gingivalis and the pathogenesis of Alzheimer's disease

Sixin Liu ¹, Catherine A Butler ², Scott Ayton ³, Eric C Reynolds ², Stuart G Dashper ²

Affiliations collapse

Affiliations

• ¹School of Dentistry, University of Michigan, Ann Arbor, United States of America.
• ²Centre for Oral Health Research, Melbourne Dental School, Bio21 Institute, The University of Melbourne, Parkville, Australia.
• ³Melbourne Dementia Research Centre, Florey Institute of Neuroscience and Mental Health, The University of Melbourne, Parkville, Australia.

• PMID: 36597758

DOI: 10.1080/1040841X.2022.2163613

Abstract

The cause of Alzheimer's disease (AD), and the pathophysiological mechanisms involved, remain major unanswered questions in medical science. Oral bacteria, especially those species associated with chronic periodontitis and particularly Porphyromonas gingivalis, are being linked causally to AD pathophysiology in a subpopulation of susceptible individuals. P. gingivalis produces large amounts of proteolytic enzymes, haem and iron capture proteins, adhesins and internalins that are secreted and attached to the cell surface and concentrated onto outer membrane vesicles (OMVs). These enzymes and adhesive proteins have been shown to cause host tissue damage and stimulate inflammatory responses. The ecological and pathophysiological roles of P. gingivalis OMVs, their ability to disperse widely throughout the host and deliver functional proteins lead to the proposal that they may be the link between a P. gingivalis focal infection in the subgingivae during periodontitis and neurodegeneration in AD. P. gingivalis OMVs can cross the blood brain barrier and may accelerate AD-specific neuropathology by increasing neuroinflammation, plaque/tangle formation and dysregulation of iron homeostasis, thereby inducing ferroptosis leading to neuronal death and neurodegeneration.