ArticleMicroorganisms2021
Bacterial Extracellular DNA Promotes β-Amyloid Aggregation.
Article in Microorganisms, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
23 citing papers in PubMed, 47 citations in OpenAlex.
- DNA Modulates Structural Transitions and Oligomerization Kinetics of the Functional Amyloid CRES.Journal of the American Chemical Society · 2026Article
- eDNA-Amyloid Synergistic Interactions in Bacterial Biofilms: A Hidden Driver of Antimicrobial Resistance.International journal of molecular sciences · 2025Review
- Regulating white blood cell activity through the novel universal receptive system.Scientific reports · 2025Article
- Modulation of Amyloid-β Aggregation by Surface Proteins from Pathogens Associated with Alzheimer's Disease.ACS chemical neuroscience · 2025Article
- Bacterial Amyloids as Hubs for Nucleic Acid Interactions: Implications and Mechanisms.International journal of molecular sciences · 2025Review
- Peripheral proteinopathy in neurodegenerative diseases.Translational neurodegeneration · 2025Review
- Universal receptive system as a novel regulator of transcriptomic activity of Staphylococcus aureus.Microbial cell factories · 2025Article
- Dietary Strategies to Mitigate Alzheimer's Disease: Insights into Antioxidant Vitamin Intake and Supplementation with Microbiota-Gut-Brain Axis Cross-Talk.Antioxidants (Basel, Switzerland) · 2024Review
- A Perspective on How Fibrinaloid Microclots and Platelet Pathology May be Applied in Clinical Investigations.Seminars in thrombosis and hemostasis · 2024Review
- Amyloid, Crohn's disease, and Alzheimer's disease - are they linked?Frontiers in cellular and infection microbiology · 2024Review
- The oral-brain axis: can periodontal pathogens trigger the onset and progression of Alzheimer's disease?Frontiers in microbiology · 2024Review
- Biological agents and the aging brain: glial inflammation and neurotoxic signaling.Frontiers in aging · 2023Review
- Virus-Like Cytosolic and Cell-Free Oxidatively Damaged Nucleic Acids Likely Drive Inflammation, Synapse Degeneration, and Neuron Death in Alzheimer's Disease.Journal of Alzheimer's disease reports · 2023Review
- Enterovirus infection and its relationship with neurodegenerative diseases.Memorias do Instituto Oswaldo Cruz · 2023Article
- Evidence supportive of a bacterial component in the etiology for Alzheimer's disease and for a temporal-spatial development of a pathogenic microbiome in the brain.Frontiers in cellular and infection microbiology · 2023Article
- Bacterial DNAemia in Alzheimer's Disease and Mild Cognitive Impairment: Association with Cognitive Decline, Plasma BDNF Levels, and Inflammatory Response.International journal of molecular sciences · 2022Article
- Novel prokaryotic system employing previously unknown nucleic acids-based receptors.Microbial cell factories · 2022Article
- Neuroinflammation in neurodegenerationFrontiers in immunology · 2022Review
- Implications of Gut Microbiota in Neurodegenerative Diseases.Frontiers in immunology · 2022Review
- The Citrullination-Neutrophil Extracellular Trap Axis in Chronic Diseases.Journal of innate immunity · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease is associated with prion-like aggregation of the amyloid β (Aβ) peptide and the subsequent accumulation of misfolded neurotoxic aggregates in the brain. Therefore, it is critical to clearly identify the factors that trigger the cascade of Aβ misfolding and aggregation. Numerous studies have pointed out the association between microorganisms and their virulence factors and Alzheimer's disease; however, their exact mechanisms of action remain unclear. Recently, we discovered a new pathogenic role of bacterial extracellular DNA, triggering the formation of misfolded Tau aggregates. In this study, we investigated the possible role of DNA extracted from different bacterial and eukaryotic cells in triggering Aβ aggregation in vitro. Interestingly, we found that the extracellular DNA of some, but not all, bacteria is an effective trigger of Aβ aggregation. Furthermore, the acceleration of Aβ nucleation and elongation can vary based on the concentration of the bacterial DNA and the bacterial strain from which this DNA had originated. Our findings suggest that bacterial extracellular DNA might play a previously overlooked role in the Aβ protein misfolding associated with Alzheimer's disease pathogenesis. Moreover, it highlights a new mechanism of how distantly localized bacteria can remotely contribute to protein misfolding and diseases associated with this process. These findings might lead to the use of bacterial DNA as a novel therapeutic target for the prevention and treatment of Alzheimer's disease.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.