Porphyromonas gingivalis in Alzheimer’s disease brains: Evidence for disease causation and treatment with small-molecule inhibitors

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Porphyromonas gingivalis in Alzheimer’s disease brains: Evidence for disease causation and treatment with small-molecule inhibitors

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Porphyromonas gingivalis in Alzheimer’s disease brains: Evidence for disease causation and treatment with small-molecule inhibitors

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Abstract

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Porphyromonas gingivalis, the keystone pathogen in chronic periodontitis, was identified in the brain of Alzheimer’s disease patients. Toxic proteases from the bacterium called gingipains were also identified in the brain of Alzheimer’s patients, and levels correlated with tau and ubiquitin pathology. Oral P. gingivalis infection in mice resulted in brain colonization and increased production of Aβ1–42, a component of amyloid plaques. Further, gingipains were neurotoxic in vivo and in vitro, exerting detrimental effects on tau, a protein needed for normal neuronal function. To block this neurotoxicity, we designed and synthesized small-molecule inhibitors targeting gingipains. Gingipain inhibition reduced the bacterial load of an established P. gingivalis brain infection, blocked Aβ1–42 production, reduced neuroinflammation, and rescued neurons in the hippocampus. These data suggest that gingipain inhibitors could be valuable for treating P. gingivalis brain colonization and neurodegeneration in Alzheimer’s disease.

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Figure legend:

Figure 5. Human cerebral cortex was left untreated or treated with TrueBlack®, then stained with CF®488A anti-NeuN (neuronal nuclei, green) and DAPI (all nuclei, blue). The sections were imaged in all channels. In untreated tissue, lipofuscin granules appear white in the merged image (left). TrueBlack® pre-treatment quenches lipofusin without affecting specific staining (right).

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In this study, the TrueBlack® Lipofuscin Autofluorescence Quencher is used to reduce background fluorescene caused by the autofluorescene tissue , Lipofuscin. Learn more about TrueBlack® Lipofuscin Autofluorescence Quencher.

DOI:

doi:10.1126/sciadv.aau3333[/vc_column_text][/vc_column][/vc_row][vc_row][vc_column][vc_column_text css=”.vc_custom_1598017023330{margin-bottom: 0px !important;}”]

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