ArticleJournal of neurochemistry2021
Receptor for advanced glycation end products up-regulation in cerebral endothelial cells mediates cerebrovascular-related amyloid β accumulation after Porphyromonas gingivalis infection.
Article in Journal of neurochemistry, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 1 of them a synthesis that pooled it.
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Who cites it
48 citing papers in PubMed, 1 synthesis or guideline pooled it, 70 citations in OpenAlex.
- How Periodontitis or Periodontal Bacteria Can Influence Alzheimer's Disease Features? A Systematic Review of Pre-Clinical Studies.Journal of Alzheimer's disease : JAD · 2023Pooled it
- Oral-Systemic Links: A Narrative Review of the Role of Periodontitis in Alzheimer's Disease Development.Cureus · 2026Review
- Reexamining the Role of Amyloid β Clearance from the Brain: Exporting Labile Iron from the Interstitial Fluid Performs a Protective Function.International journal of molecular sciences · 2026Review
- Unveiling the Impact ofJournal of the American Heart Association · 2026Article
- Association between Alzheimer's disease andWorld journal of biological chemistry · 2025Article
- Oral diseases as emerging risk factors for Alzheimer's disease: A scoping review.The Japanese dental science review · 2025Review
- Targeting the awry Aβ pathway in Alzheimer's disease: hype and hurdles.Inflammopharmacology · 2025Review
- Brain activation generated by periodontal initial treatment.Journal of dental sciences · 2025Article
- The role of oral microbiota in lung carcinogenesis through the oral-lung axis: a comprehensive review of mechanisms and therapeutic potential.Discover oncology · 2025Review
- Effect of natural compounds on NRF2/KEAP1 signaling in periodontitis: a potential use to prevent age-related disorders.Molecular biology reports · 2025Review
- Unraveling brain aging through the lens of oral microbiota.Neural regeneration research · 2025Article
- Salivaomics: New Frontiers in Studying the Relationship Between Periodontal Disease and Alzheimer's Disease.Metabolites · 2025Review
- Multi-organ frailty is enhanced by periodontitis-induced inflammaging.Inflammation and regeneration · 2025Article
- Exploring the Link Between Periodontitis and Alzheimer's Disease-Could a Nanoparticulate Vaccine Break It?Pharmaceutics · 2025Review
- Alzheimer's Disease andLife (Basel, Switzerland) · 2025Review
- Smoking Impacts Alzheimer's Disease Progression Through Oral Microbiota Modulation.Molecular neurobiology · 2025Review
- Amyloid-β and heart failure in Alzheimer's disease: the new vistas.Frontiers in medicine · 2025Review
- A Comprehensive Review on Preclinical Alzheimer's Disease Models: Evaluating their Clinical Relevance.Current pharmaceutical biotechnology · 2025Review
- Endothelial Dysfunctions in Blood-Brain Barrier Breakdown in Alzheimer's Disease: From Mechanisms to Potential Therapies.CNS neuroscience & therapeutics · 2024Review
- Loss of Direct Vascular Contact to Astrocytes in the Hippocampus as an Initial Event in Alzheimer's Disease. Evidence from Patients, In Vivo and In Vitro Experimental Models.Molecular neurobiology · 2024Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cerebrovascular-related amyloidogenesis is found in over 80% of Alzheimer's disease (AD) cases, and amyloid β (Aβ) generation is increased in the peripheral macrophages during infection of Porphyromonas gingivalis (P. gingivalis), a causal bacterium for periodontitis. In this study, we focused on receptor for advanced glycation end products (RAGE), the key molecule involves in Aβ influx after P. gingivalis infection to test our hypothesis that Aβ transportation from periphery into the brain, known as "Aβ influx," is enhanced by P. gingivalis infection. Using cultured hCMEC/D3 cell line, in comparison to uninfected cells, directly infection with P. gingivalis (multiplicity of infection, MOI = 5) significantly increased a time-dependent RAGE expression resulting in a dramatic increase in Aβ influx in the hCMEC/D3 cells; the P. gingivalis-up-regulated RAGE expression was significantly decreased by NF-κB and Cathepsin B (CatB)-specific inhibitors, and the P.gingivalis-increased IκBα degradation was significantly decreased by CatB-specific inhibitor. Furthermore, the P. gingivalis-increased Aβ influx was significantly reduced by RAGE-specific inhibitor. Using 15-month-old mice (C57BL/6JJmsSlc, female), in comparison to non-infection mice, systemic P. gingivalis infection for three consecutive weeks (1 × 10
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