Periodontal Inflammation and Dysbiosis: Contributors to Alzheimer's Disease

Abstract

Alzheimer’s disease is a continuum condition characterized by specific pathologies such as amyloid β plaques (Aβ), neurofibrillary tangles, inflammation, and neurodegeneration. There is consensus that the preclinical phase in which there is AD pathology but no symptomatology could be the appropriate phase to target AD pathology with preventive measures. Therefore, an important focus is placed on identifying modifiable risks for AD and other dementia before severe irreversible brain damage occurs. Recent studies show that peripheral inflammation and microbes play a crucial role in AD pathogenesis by inducing neuroinflammation, brain pathology, and cognitive decline. Periodontal disease a localized peripheral chronic inflammatory condition affecting about 50% of people over 55 years of age is characterized by dysbiosis (microbial imbalance) with high Gram-negative pathogenic bacterial load and increased systemic inflammation. We posed that periodontal disease with its significant local and systemic inflammatory and microbial burden contribute to AD pathogenesis. Literature data including results coming from our group will show support for periodontal disease cont ribution to AD brain pathology.