INTRODUCTION

Alzheimer’s disease (AD) patients exhibit neuroinflammation consistent with infection, including microglial activation, inflammasome activation, complement activation, and altered cytokine profiles (12). Infectious agents have been found in the brain and postulated to be involved with AD, but robust evidence of causation has not been established (3). The recent characterization of amyloid-β (Aβ) as an antimicrobial peptide has renewed interest in identifying a possible infectious cause of AD (46).

Chronic periodontitis (CP) and infection with Porphyromonas gingivalis—a keystone pathogen in the development of CP (7)have been identified as significant risk factors for developing Aβ plaques, dementia, and AD (812). A…



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