Periodontitis as a risk factor for Alzheimer’s disease – the experimental journey so far; with hope of therapy

Abstract

Periodontitis and Alzheimer’s disease (AD) exist globally within the adult population. Given that the risk of AD incidence doubles within ten years from the time of periodontal disease diagnosis, there is a window of opportunity for slowing down or preventing AD by risk reduction based intervention. Literature appraisal on the shared risk factors of these diseases suggests a shift to a healthy lifestyle would be beneficial. Generalised (chronic) periodontitis with an established dysbiotic polymicrobial aetiology, affects the tooth supporting tissues with eventual tooth loss. The cause of AD remains unknown, however two neurohistopathological lesions – amyloid-beta plaques and neurofibrillary tangles, together with the clinical history, provide AD diagnosis at autopsy. Historically, prominence was given to the two hallmark lesions but now empha-sis is placed on cerebral inflammation and what triggers it. Low so-cioeconomic status promotes poor lifestyles that compromise oral and personal hygiene along with reliance on poor dietary intake. Taken together with advancing age and a declining immune protec-tion, these risk factors may negatively impact on periodontitis and AD. These factors also provide a tangible solution to controlling pathogenic bacteria indigenous to the oral and gastrointestinal tract microbiomes in vulnerable subjects. The focus here is on Porphy-romonas gingivalis, one of several important bacterial pathogens associated with both periodontitis and AD. Recent research has en-abled advances in our knowledge of the armoury of P. gingivalis via reproduction of all clinical and neuropathological hallmark le-sions of AD and chronic periodontal disease in vitro and in vivo ex-perimental models, thus paving the way for better future manage-ment.