| Summary: | Amyloid-β (Aβ)-peptide production or deposition in the neuropathology of Alzheimer’s disease (AD) was shown to be caused by chronic inflammation that may be induced by infection, but the role of pathogenic-bacteria-related AD-associated Aβ is not yet clearly understood. In this study, we validated the hypothesis that there is a correlation between the Aβ-protein load and bacterial infection and that there are effects of bacteria, <i>Staphylococcus aureus</i> (<i>S. aureus</i>), on the Aβ load in the inflammatory environment of human tonsils. Here, we detected Aβ-peptide deposits in human tonsil tissue as well as tissue similar to tonsilloliths found in the olfactory cleft. Interestingly, we demonstrated for the first time the presence of <i>Staphylococcus aureus</i> (<i>S. aureus</i>) clustered around or embedded in the Aβ deposits. Notably, we showed that treatment with <i>S. aureus</i> upregulated the Aβ-protein load in cultures of human tonsil organoids and brain organoids, showing the new role of <i>S. aureus</i> in Aβ-protein aggregation. These findings suggest that a reservoir of Aβ and pathogenic bacteria may be a possible therapeutic target in human tonsils, supporting the treatment of antibiotics to prevent the deposition of Aβ peptides via the removal of pathogens in the intervention of AD pathogenesis.
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