Connection between periodontitis and Alzheimer's disease: possible roles of microglia and leptomeningeal cells

J Pharmacol Sci. 2014;126(1):8-13. doi: 10.1254/jphs.14r11cp. Epub 2014 Aug 29.

Abstract

Neuroinflammation, inflammation of the brain, is strongly implicated in Alzheimer's disease (AD), which can be enhanced by systemic inflammation. Therefore, the initiation and progression of AD are affected by systemic diseases such as cardiovascular disease and diabetes. This concept suggests a possible link between periodontitis and AD because periodontitis is a peripheral, chronic infection that elicits a significant systemic inflammatory response. There is now growing clinical evidence that chronic periodontitis is closely linked to the initiation and progression of AD. Recent studies have suggested that leptomeningeal cells play an important role in transducing systemic inflammatory signals to the brain-resident microglia, which in turn initiate neuroinflammation. Furthermore, it is apparent that senescent-type microglia respond in an exaggerated manner to systemic inflammation. It is estimated that a high percentage of adults are suffering from periodontitis, and the prevalence of periodontitis increases with age. Therefore, chronic periodontitis can be a significant source of covert systemic inflammation within the general population. The present review article highlights our current understanding of the link between periodontitis and AD.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Alzheimer Disease / etiology*
  • Alzheimer Disease / metabolism
  • Amyloid beta-Peptides / metabolism
  • Brain / cytology*
  • Chronic Disease
  • Humans
  • Inflammation / etiology
  • Lipopolysaccharides
  • Meninges / cytology*
  • Meninges / physiology*
  • Microglia / pathology
  • Microglia / physiology*
  • Periodontitis / complications*
  • Periodontitis / microbiology
  • Phosphorylation
  • Porphyromonas gingivalis / pathogenicity
  • Risk Factors
  • tau Proteins / metabolism

Substances

  • Amyloid beta-Peptides
  • Lipopolysaccharides
  • tau Proteins