Porphyromonas gingivalis infection may contribute to systemic and intracerebral amyloid-beta: implications for Alzheimer's disease onset.

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.