Porphyromonas gingivalis in Alzheimer’s disease brains: Evidence for disease causation and treatment with small-molecule inhibitors
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Gingipains from Porphyromonas gingivalis drive Alzheimer’s pathology and can be blocked with small-molecule inhibitors.
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Loss of function variation in TREM1 is responsible for defective clearance of P. gingivalis and gingipains from the brain, resulting in chronic, low-level infection and neuroinflammation in susceptible individuals.
“Moreover, loss of function variation in TREM1 was indicated to be responsible for the defective clearance of P. gingivalis and gingipains from the brain, resulting in chronic, low-level infection and neuroinflammation in susceptible individuals.155”
From Role of neuroinflammation in neurodegeneration development (2023) · cites this paper as [155]
The Discussion (page not provided) proposes that polymorphisms in innate immune genes may impair clearance of P. gingivalis and gingipains, leading to chronic infection and neuroinflammation. It also suggests that a TREM1-associated allele might reduce the response to infection, but does not establish that loss-of-function TREM1 variation is responsible for defective clearance. (LLM, conf=0.88)
Experimental — accuracy not yet measuredIncreased levels of P. gingivalis proteins have been found in the brains of AD individuals compared to non-demented, healthy control subjects.
“Increased levels of P. gingivalis proteins have been found in the brains of AD individuals compared to non-demented, healthy control subjects [72].”
From What would it take to prove that a chronic infection is a causal agent in Alzheimer’s disease? (2025) · cites this paper as [72]
Porphyromonas gingivalis and its gingipain proteases contribute to Alzheimer's disease pathogenesis through yet unclear mechanisms.
“Porphyromonas gingivalis (Pg) and its gingipain proteases contribute to Alzheimer’s disease (AD) pathogenesis through yet unclear mechanisms.”
From Oral Microbially-Induced Small Extracellular Vesicles Cross the Blood–Brain Barrier (2024) · cites this paper as [6]
There is a strong epidemiologic association between periodontitis and Alzheimer's disease and related dementia.
“There is a strong epidemiologic association between periodontitis (PD) and ADRD [5,6,7,8,9,10,11,12,13] but how these two diseases intersect and whether it is at the level of causation is unclear.”
From Oral Microbially-Induced Small Extracellular Vesicles Cross the Blood–Brain Barrier (2024) · cites this paper as [6]
Gingipains have been detected in the brains of Alzheimer's disease patients postmortem.
“In addition, gingipains, proteolytic enzymes of the keystone oral pathogen Porphyromonas gingivalis (Pg), have been detected in the brains of AD patients postmortem [6].”
From Oral Microbially-Induced Small Extracellular Vesicles Cross the Blood–Brain Barrier (2024) · cites this paper as [6]
Oral P. gingivalis infection increases Aβ42 generation, where Aβ42 can also be toxic to P. gingivalis.
“Oral P. gingivalis infection increases Aβ42 generation, where Aβ42 can also be toxic to P. gingivalis [537].”
From Molecular and cellular mechanisms underlying the pathogenesis of Alzheimer’s disease (2020) · cites this paper as [537]
Inhibition of Gingipain reduces P. gingivalis brain infection and consequent toxic effects in the hippocampus.
“In addition, inhibition of Gingipain, a virulence factor produced by P. gingivalis can effectively reduce P. gingivalis brain infection and the consequent toxic effects in the hippocampus [537].”
From Molecular and cellular mechanisms underlying the pathogenesis of Alzheimer’s disease (2020) · cites this paper as [537]
Oral Porphyromonas gingivalis infection in wild-type mice elevates intraparenchymal Aβ, and gingipain inhibition reduces bacterial burden, Aβ levels, and neuroinflammation.
“Oral infection of WT mice with Porphyromsonas gingivalis resulted in elevated intraparenchymal Aβ levels, and inhibition of gingipain activity led to reduced intracerebral bacterial burden, decreased Aβ levels and reduced neuroinflammation (Dominy et al., 2019).”
From Alzheimer Disease: An Update on Pathobiology and Treatment Strategies (2019) · cites this paper as Dominy et al., 2019
Periodontal bacterial proteins and DNA are present in human Alzheimer disease brain.
“In this study, periodontal bacterial proteins (gingipains) and DNA were identified in human AD brain.”
From Alzheimer Disease: An Update on Pathobiology and Treatment Strategies (2019) · cites this paper as Dominy et al., 2019
The interplay between the bacterial burden and host response is the most plausible biological mechanism linking periodontitis to a number of chronic systemic diseases, such as diabetes mellitus, cardiovascular diseases, and neurological diseases such as Alzheimer.
“The interplay between the bacterial burden and host response is the most plausible biological mechanism linking periodontitis to a number of chronic systemic diseases, such as diabetes mellitus, CVDs, and neurological diseases such as Alzheimer.17,19,20”
From Periodontitis is associated with hypertension: a systematic review and meta-analysis (2020) · cites this paper as [20]
Porphyromonas gingivalis and periodontal disease have been identified as significant risk factors for the development of amyloid beta plaques, dementia, and Alzheimer's disease.
“Porphyromonas gingivalis and periodontal disease have also been identified as significant risk factors for the development of amyloid beta plaques, dementia, and Alzheimer's disease.213”
From The oral microbiome: Role of key organisms and complex networks in oral health and disease (2021) · cites this paper as [213]
Gingipains colocalize with tau protein, a protein in the brain which becomes misfolded and insoluble in patients with Alzheimer's disease.
“Gingipains colocalize with tau protein, a protein in the brain which becomes misfolded and insoluble in patients with Alzheimer's disease.”
From The oral microbiome: Role of key organisms and complex networks in oral health and disease (2021) · cites this paper as [213]
A diagnosis of Alzheimer's disease correlates with the gingipain load in the brain and also with other P gingivalis-specific virulence factors, including P gingivalis lipopolysaccharide.
“A diagnosis of Alzheimer's disease correlates with the gingipain load in the brain and also with other P gingivalis‐specific virulence factors, including P gingivalis lipopolyaccharide.”
From The oral microbiome: Role of key organisms and complex networks in oral health and disease (2021) · cites this paper as [213]
Gingipains cleave tau protein and contribute to tau tangle formation resulting disease.
“It has now been demonstrated that gingipains cleave tau protein and contribute to tau tangle formation resulting disease.”
From The oral microbiome: Role of key organisms and complex networks in oral health and disease (2021) · cites this paper as [213]
Gingipains, another virulence factor of P gingivalis, are implicated in Alzheimer's disease pathology.
“Gingipains, another virulence factor of P gingivalis, are implicated in Alzheimer's disease pathology.”
From The oral microbiome: Role of key organisms and complex networks in oral health and disease (2021) · cites this paper as [213]
Studies in mice have shown that oral P gingivalis consistently invades the brain in a gingipain-assisted manner, and that injection of gingipains into the brain increases neuronal degeneration to a level higher than that found in controls.
“Studies in mice have shown that oral P gingivalis consistently invades the brain in a gingipain‐assisted manner, and that injection of gingipains into the brain increases neuronal degeneration to a level higher than that found in controls.213”
From The oral microbiome: Role of key organisms and complex networks in oral health and disease (2021) · cites this paper as [213]
The altered microbiota of patients could transfer the disease from a human host to a mouse host.
“Of extreme relevance, the altered microbiota of patients could transfer the disease from a human host to a mouse host (113, 116–120).”
From The gut-brain axis: how microbiota and host inflammasome influence brain physiology and pathology (2020) · cites this paper as [120]
Porphyromonas gingivalis and gingipains were identified in the brain of AD patients but not in the brain of control patients with no history of neurological abnormality or condition.
“Dominy SS. and colleagues identified Porphyromonas gingivalis and the gingipains, the toxic proteases produced by this bacterium, in the brain of AD patients but not in the brain of control patients with no history of any neurological abnormality or condition (120).”
From The gut-brain axis: how microbiota and host inflammasome influence brain physiology and pathology (2020) · cites this paper as [120]
Gingipains co-localized with neurons, astrocytes, tau tangles, and intraneuronal Aβ in AD patient tissue.
“Gingipains co-localized with neurons and astrocytes and also tau tangles and intraneuronal Aβ in the tissue of AD patients (120).”
From The gut-brain axis: how microbiota and host inflammasome influence brain physiology and pathology (2020) · cites this paper as [120]
P. gingivalis 16S rRNA was detected in both the cerebrospinal fluid and the cerebral cortex of AD patients.
“P. gingivalis 16S rRNA was detected in both the cerebrospinal fluid and in the cerebral cortex of AD patients (120).”
From The gut-brain axis: how microbiota and host inflammasome influence brain physiology and pathology (2020) · cites this paper as [120]
Porphyromonas gingivalis, the causing agent of chronic periodontitis, has a role in the etiology of AD.
“To conclude, an intriguing and relevant role of the oral pathogen Porphyromonas gingivalis, the causing agent of chronic periodontitis, has been elucidated in the etiology of AD (120).”
From The gut-brain axis: how microbiota and host inflammasome influence brain physiology and pathology (2020) · cites this paper as [120]
Mice that received gingipains-deficient P. gingivalis or synthetic gingipains inhibitors had significantly less P. gingivalis DNA detectable in the brain, less Aβ production, reduced neuroinflammation, and increased number of healthy neurons in the hippocampus.
“On the other hand, mice that received gingipains-deficient P. gingivalis or synthetic gingipains inhibitors had significantly less P. gingivalis DNA detectable in the brain, less Aβ production, reduced neuroinflammation, and increased number of healthy neurons in the hippocampus (120).”
From The gut-brain axis: how microbiota and host inflammasome influence brain physiology and pathology (2020) · cites this paper as [120]
Oral P. gingivalis infection in mice not genetically susceptible to AD resulted in detection of P. gingivalis DNA in the brain and remarkably increased production of Aβ deposits.
“The oral P. gingivalis infection in mice that are not genetically susceptible to develop AD resulted in the detection of P. gingivalis DNA in the brain and remarkably increased production of Aβ deposits (120).”
From The gut-brain axis: how microbiota and host inflammasome influence brain physiology and pathology (2020) · cites this paper as [120]
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Dose-Response Meta-Analysis on Tooth Loss With the Risk of Cognitive Impairment and Dementia
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Outer Membrane Vesicles: Biogenesis, Functions, and Issues
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The Immunopathogenesis of Alzheimer’s Disease Is Related to the Composition of Gut Microbiota
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Parkinson’s Disease: A Systemic Inflammatory Disease Accompanied by Bacterial Inflammagens
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Molecular Strategies Underlying Porphyromonas gingivalis Virulence
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The interaction between ageing and Alzheimer's disease: insights from the hallmarks of ageing
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Distal Consequences of Oral Inflammation
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Periodontitis: An Oral Disease with Severe Consequences
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- Authors
- Dominy, S. S., Lynch, C., Ermini, F., Benedyk, M., Marczyk, A., Konradi, A., Nguyen, M., Haditsch, U., Raha, D., Griffin, C., Holsinger, L. J., Arastu-Kapur, S., Kaba, S., Lee, A., Ryder, M. I., Potempa, B., Mydel, P., Hellvard, A., Adamowicz, K., Hasturk, H., Walker, G. D., Reynolds, E. C., Faull, R. L. M., Curtis, M. A., Dragunow, M., & Potempa, J.
- Affiliations
- Cortexyme, Inc., 269 East Grand Ave., South San Francisco, CA, USA.
- Department of Microbiology, Faculty of Biochemistry, Biophysics and Biotechnology, Jagiellonian University, Krakow, Poland.
- Jagiellonian University (PL)
- University of California, San Francisco (US)
- University of Louisville (US)
- The Forsyth Institute, Cambridge, MA, USA.
- The University of Melbourne (AU)
- University of Auckland (NZ)
- Corresponding author
- Dominy, Stephen S.
- Lynch, Casey
- Potempa, Jan
- ORCID
- Venue
- Science Advances
- Published
- 2019-01-04
- Volume
- 5
- Issue
- 1
- Pages
- eaau3333-eaau3333
- ISSN
- 2375-2548 (ISSN-L)
- PMC
- PMC6357742
- OpenAlex
- W2912555658
- Cited by
- 1,966
- References
- 108
- Citations by year
- 2026: 243 · 2025: 301 · 2024: 262 · 2023: 256 · 2022: 230 · 2021: 278 · 2020: 271 · 2019: 120 · 2018: 1 · 2016: 1
- FWCI
- 154.08
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- cc-by
- Locations
- Science Advances (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Homo Politicus (Academy of Humanities and Economics in Lodz) (submittedVersion, cc-by-nc-nd)
- Minerva Access (University of Melbourne) (submittedVersion, cc-by)
- eScholarship (California Digital Library) (submittedVersion)
- eScholarship (California Digital Library) (submittedVersion, cc-by)
- Funders
- Cortexyme, Inc. (N/A)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Dentistry › Periodontics › Oral microbiology and periodontitis research
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- Porphyromonas gingivalis, Alzheimer's disease, gingipains, bacterial virulence factors, small molecule inhibitors, etiology, neuroinflammation, periodontal pathogens
- MeSH terms
- Gingipain Cysteine Endopeptidases, Aged, Alzheimer Disease, Animals, Brain, Disease Models, Animal, Female, Humans, Male, Mice, Inbred BALB C, Middle Aged, Peptide Fragments, Pilot Projects, Prospective Studies, Saliva, Amyloid beta-Peptides, Bacteroidaceae Infections, tau Proteins, Porphyromonas gingivalis, Neuroprotective Agents, Cell Line, Tumor, Mice, Small Molecule Libraries
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