Open Access Online OnlyReviewDOI: 10.3238/dzz-int.2021.0014Pages 121, Language: EnglishAarabi, Ghazal / Thomalla, Götz / Walther, Carolin / Mayer, Carola / Beikler, Thomas / Heydecke, Guido / Seedorf, UdoIntroduction: Neuroinflammation is a hallmark of Alzheimer's disease (AD). Multiple infectious agents have been demonstrated in the brain and proposed to be involved in AD, but robust evidence of causation has not yet been established. It was hypothesized that periodontitis (PD) and infection with Porphyromonas gingivalis may be linked to onset and progression of AD. Although inflammation is present in both diseases, the exact mechanisms and interactions between periodontitis and AD are poorly understood.
Method: In this narrative review, we highlight recent progress in exploring potential associations of PD with AD and its surrogates (amyloid plaques) and clinical sequelae (i.e. dementia), respectively.
Discussion and Result: Recent evidence suggests that periodontitis interacts with AD to increase the severity of clinical dementia and to accelerate its manifestations. These results indicate that periodontitis may be an emerging risk factor for AD and that the risk may be mediated directly by Porphyromonas gingivalis and its secreted neurotoxic gingipains. The recent development of an oral gingipain inhibitor, which is currently tested in a randomized controlled trial, offers the unique opportunity to verify the infectious hypothesis of AD. If successful, this research can be expected to result in a significant improvement of prevention and treatment of PD and AD.
Keywords: Alzheimer's disease, Porphyromonas gingivalis, dementia, gingipain, neuroinflammation, oral prophylaxis, periodontitis, therapy