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.2015 Sep 17:7:29143.
doi: 10.3402/jom.v7.29143. eCollection 2015.

Can oral infection be a risk factor for Alzheimer's disease?

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Can oral infection be a risk factor for Alzheimer's disease?

Ingar Olsen et al. J Oral Microbiol..

Abstract

Alzheimer's disease (AD) is a scourge of longevity that will drain enormous resources from public health budgets in the future. Currently, there is no diagnostic biomarker and/or treatment for this most common form of dementia in humans. AD can be of early familial-onset or sporadic with a late-onset. Apart from the two main hallmarks, amyloid-beta and neurofibrillary tangles, inflammation is a characteristic feature of AD neuropathology. Inflammation may be caused by a local central nervous system insult and/or by peripheral infections. Numerous microorganisms are suspected in AD brains ranging from bacteria (mainly oral and non-oral Treponema species), viruses (herpes simplex type I), and yeasts (Candida species). A causal relationship between periodontal pathogens and non-oral Treponema species of bacteria has been proposed via the amyloid-beta and inflammatory links. Periodontitis constitutes a peripheral oral infection that can provide the brain with intact bacteria and virulence factors and inflammatory mediators due to daily, transient bacteremias. If and when genetic risk factors meet environmental risk factors in the brain, disease is expressed, in which neurocognition may be impacted, leading to the development of dementia. To achieve the goal of finding a diagnostic biomarker and possible prophylactic treatment for AD, there is an initial need to solve the etiological puzzle contributing to its pathogenesis. This review therefore addresses oral infection as the plausible etiology of late-onset AD (LOAD).

Keywords: Alzheimer's disease; direct cause; microorganisms; oral bacteria; pathogenesis.

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Figures

Fig. 1
Fig. 1
The pathological hallmarks of AD, numerous extracellular amyloid-Aβ plaques and intra-neuronal neurofibrillary tangles (NFTs). Although there are several NFTs, only one is picked out in boxes at 10× and 40× objective lens magnification.
Fig. 2
Fig. 2
Immunofluorescence labeling (green dots) of hippocampal CA neurons opsonized by iC3b following monoinfection withP. gingivalis at 24 weeks ofAPOɛ gene knockout (ApoE−/ −) mice. This is indirect evidence of an oral infection having affected the host's brain.
Fig. 3
Fig. 3
Section of pons area of Alzheimer's disease brain from an 84-year-old female subject (from Ref. (5) with permission), demonstrates metabolically activeTreponema pectinovorum oral bacteria (arrows) stained dark blue following immunostaining with anti-T. pectinovorum using the avidin–biotin peroxidase method.
See this image and copyright information in PMC

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