Porphyromonas gingivalis infection may contribute to systemic and intracerebral amyloid-beta: Implications for Alzheimer’s disease onset

Olsen, Ingar and Singhrao, Simarjit Kaur orcid iconORCID: 0000-0001-9573-5963 (2020) Porphyromonas gingivalis infection may contribute to systemic and intracerebral amyloid-beta: Implications for Alzheimer’s disease onset. Expert Review of Anti-infective Therapy, 18 (11). pp. 1063-1066. ISSN 1478-7210

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Official URL: https://doi.org/10.1080/14787210.2020.1792292

Abstract

The microbiota of “chronic” periodontitis, particularly Porphyromonas gingivalis, have been implicated in Alzheimer’s disease (AD) because this bacterium has a range of enzymes (cathepsin B and gingipains) that are shown to interact with the amyloid precursor protein (APP) and neuronal tau resulting in the formation of amyloid-beta (Aβ) and neurofibrillary tangles (NFTs). These two lesions remain pivotal to explaining AD pathogenesis alongside of clinical symptoms. Deposits of Aβ in the brain can start 10-20 years before the clinical symptoms of cognitive decline and the diagnosis of AD is established. It is rarely mentioned that the AD risk doubles if the individual has received a diagnosis of periodontitis for around 10 years. This editorial is a review of recent but salient literature supporting the idea that periodontal disease can contribute to a systemic Aβ pool that may enter the brain over time. In addition, intracerebral production of Aβ can be initiated by P. gingivalis, which occurs via host and bacterially derived cathepsin B acting as β-secretase to process the APP via the amyloidogenic pathway yielding Aβ3-42. These findings support a systemic and an intracerebral Aβ contribution from “chronic” periodontitis in subsequent AD development.


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